TY  - JOUR
AU  - Pépin, Marion
AU  - Klimkowicz-Mrowiec, Aleksandra
AU  - Godefroy, Olivier
AU  - Delgado, P.
AU  - Carriazo, S.
AU  - Ferreira, A.C.
AU  - Golenia, A.
AU  - Malyszko, J.
AU  - Grodzicki, T.
AU  - Giannakou, K.
AU  - Paolisso, G.
AU  - Barbieri, M.
AU  - Garneata, L.
AU  - Mocanu, C.A.
AU  - Liabeuf, S.
AU  - Spasovski, G.
AU  - Zoccali, C.
AU  - Bruchfeld, A.
AU  - Farinha, A.
AU  - Arici, M.
AU  - Capasso, G.
AU  - Wiecek, A.
AU  - Massy, Z.A.
AU  - Andrade, A.
AU  - Bachmann, M.
AU  - Bumblyte, I.
AU  - Covic, A.C.
AU  - Endlich, N.
AU  - Engvig, A.
AU  - Fouque, D.
AU  - Franssen, C.
AU  - Frische, S.
AU  - Gesualdo, L.
AU  - Goumenos, D.
AU  - Mani, L.-Y.
AU  - Marti, H.-P.
AU  - Mayer, C.
AU  - Nielsen, R.
AU  - Pešić, Vesna
AU  - Rroji, M.
AU  - Sakkas, G.
AU  - Stevens, K.
AU  - Vazelov, E.
AU  - Viggiano, D.
AU  - Zacharia, L.
AU  - Hoorn, E.
AU  - Figurek, A.
AU  - Unwin, R.
AU  - Wagner, C.A.
AU  - Wanner, C.
AU  - Nitsch, D.
AU  - Fridolin, I.
AU  - Hafez, G.
AU  - Soler Romeo, M.J.
AU  - Batinić, Bojan
AU  - Carrasco, L.
AU  - Gansevoort, R.
AU  - Martino, G.
AU  - Mattace Raso, F.
AU  - Nistor, I.
AU  - Ortiz, A.
AU  - Rastenytė, D.
AU  - Stefan, G.
AU  - Tedeschi, G.
AU  - Bikbov, B.
AU  - Endlich, K.H.
AU  - Kurganaite, J.
AU  - Perico, N.
AU  - Remuzzi, G.
AU  - Trepiccione, F.
AU  - Blankestijn, P.
AU  - Eckardt, K.-U.
AU  - Fliser, D.
AU  - Gutiérrez-Jiménez, E.
AU  - Konig, M.
AU  - Rychlik, I.
AU  - Deleidi, M.
AU  - Reusz, G.
AU  - Farisco, M.
AU  - Imenez Silva, P.H.
AU  - Bobot, M.
AU  - Capolongo, G.
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5594
AB  - Background: Cognitive impairment is common in patients with chronic kidney disease (CKD), and early intervention may prevent the progression of this condition. Methods: Here, we review interventions for the complications of CKD (anemia, secondary hyperparathyroidism, metabolic acidosis, harmful effects of dialysis, the accumulation of uremic toxins) and for prevention of vascular events, interventions that may potentially be protective against cognitive impairment. Furthermore, we discuss nonpharmacological and pharmacological methods to prevent cognitive impairment and/or minimize the latter's impact on CKD patients' daily lives. Results: A particular attention on kidney function assessment is suggested during work-up for cognitive impairment. Different approaches are promising to reduce cognitive burden in patients with CKD but the availabe dedicated data are scarce. Conclusions: There is a need for studies assessing the effect of interventions on the cognitive function of patients with CKD.
PB  - John Wiley and Sons Inc
T2  - European Journal of Neurology
T1  - Cognitive disorders in patients with chronic kidney disease: Approaches to prevention and treatment
VL  - 30
IS  - 9
SP  - 2899
EP  - 2911
DO  - 10.1111/ene.15928
ER  - 

@article{
author = "Pépin, Marion and Klimkowicz-Mrowiec, Aleksandra and Godefroy, Olivier and Delgado, P. and Carriazo, S. and Ferreira, A.C. and Golenia, A. and Malyszko, J. and Grodzicki, T. and Giannakou, K. and Paolisso, G. and Barbieri, M. and Garneata, L. and Mocanu, C.A. and Liabeuf, S. and Spasovski, G. and Zoccali, C. and Bruchfeld, A. and Farinha, A. and Arici, M. and Capasso, G. and Wiecek, A. and Massy, Z.A. and Andrade, A. and Bachmann, M. and Bumblyte, I. and Covic, A.C. and Endlich, N. and Engvig, A. and Fouque, D. and Franssen, C. and Frische, S. and Gesualdo, L. and Goumenos, D. and Mani, L.-Y. and Marti, H.-P. and Mayer, C. and Nielsen, R. and Pešić, Vesna and Rroji, M. and Sakkas, G. and Stevens, K. and Vazelov, E. and Viggiano, D. and Zacharia, L. and Hoorn, E. and Figurek, A. and Unwin, R. and Wagner, C.A. and Wanner, C. and Nitsch, D. and Fridolin, I. and Hafez, G. and Soler Romeo, M.J. and Batinić, Bojan and Carrasco, L. and Gansevoort, R. and Martino, G. and Mattace Raso, F. and Nistor, I. and Ortiz, A. and Rastenytė, D. and Stefan, G. and Tedeschi, G. and Bikbov, B. and Endlich, K.H. and Kurganaite, J. and Perico, N. and Remuzzi, G. and Trepiccione, F. and Blankestijn, P. and Eckardt, K.-U. and Fliser, D. and Gutiérrez-Jiménez, E. and Konig, M. and Rychlik, I. and Deleidi, M. and Reusz, G. and Farisco, M. and Imenez Silva, P.H. and Bobot, M. and Capolongo, G.",
year = "2023",
abstract = "Background: Cognitive impairment is common in patients with chronic kidney disease (CKD), and early intervention may prevent the progression of this condition. Methods: Here, we review interventions for the complications of CKD (anemia, secondary hyperparathyroidism, metabolic acidosis, harmful effects of dialysis, the accumulation of uremic toxins) and for prevention of vascular events, interventions that may potentially be protective against cognitive impairment. Furthermore, we discuss nonpharmacological and pharmacological methods to prevent cognitive impairment and/or minimize the latter's impact on CKD patients' daily lives. Results: A particular attention on kidney function assessment is suggested during work-up for cognitive impairment. Different approaches are promising to reduce cognitive burden in patients with CKD but the availabe dedicated data are scarce. Conclusions: There is a need for studies assessing the effect of interventions on the cognitive function of patients with CKD.",
publisher = "John Wiley and Sons Inc",
journal = "European Journal of Neurology",
title = "Cognitive disorders in patients with chronic kidney disease: Approaches to prevention and treatment",
volume = "30",
number = "9",
pages = "2899-2911",
doi = "10.1111/ene.15928"
}

Pépin, M., Klimkowicz-Mrowiec, A., Godefroy, O., Delgado, P., Carriazo, S., Ferreira, A.C., Golenia, A., Malyszko, J., Grodzicki, T., Giannakou, K., Paolisso, G., Barbieri, M., Garneata, L., Mocanu, C.A., Liabeuf, S., Spasovski, G., Zoccali, C., Bruchfeld, A., Farinha, A., Arici, M., Capasso, G., Wiecek, A., Massy, Z.A., Andrade, A., Bachmann, M., Bumblyte, I., Covic, A.C., Endlich, N., Engvig, A., Fouque, D., Franssen, C., Frische, S., Gesualdo, L., Goumenos, D., Mani, L.-Y., Marti, H.-P., Mayer, C., Nielsen, R., Pešić, V., Rroji, M., Sakkas, G., Stevens, K., Vazelov, E., Viggiano, D., Zacharia, L., Hoorn, E., Figurek, A., Unwin, R., Wagner, C.A., Wanner, C., Nitsch, D., Fridolin, I., Hafez, G., Soler Romeo, M.J., Batinić, B., Carrasco, L., Gansevoort, R., Martino, G., Mattace Raso, F., Nistor, I., Ortiz, A., Rastenytė, D., Stefan, G., Tedeschi, G., Bikbov, B., Endlich, K.H., Kurganaite, J., Perico, N., Remuzzi, G., Trepiccione, F., Blankestijn, P., Eckardt, K.-U., Fliser, D., Gutiérrez-Jiménez, E., Konig, M., Rychlik, I., Deleidi, M., Reusz, G., Farisco, M., Imenez Silva, P.H., Bobot, M.,& Capolongo, G.. (2023). Cognitive disorders in patients with chronic kidney disease: Approaches to prevention and treatment. in European Journal of Neurology
John Wiley and Sons Inc., 30(9), 2899-2911.
https://doi.org/10.1111/ene.15928

Pépin M, Klimkowicz-Mrowiec A, Godefroy O, Delgado P, Carriazo S, Ferreira A, Golenia A, Malyszko J, Grodzicki T, Giannakou K, Paolisso G, Barbieri M, Garneata L, Mocanu C, Liabeuf S, Spasovski G, Zoccali C, Bruchfeld A, Farinha A, Arici M, Capasso G, Wiecek A, Massy Z, Andrade A, Bachmann M, Bumblyte I, Covic A, Endlich N, Engvig A, Fouque D, Franssen C, Frische S, Gesualdo L, Goumenos D, Mani L, Marti H, Mayer C, Nielsen R, Pešić V, Rroji M, Sakkas G, Stevens K, Vazelov E, Viggiano D, Zacharia L, Hoorn E, Figurek A, Unwin R, Wagner C, Wanner C, Nitsch D, Fridolin I, Hafez G, Soler Romeo M, Batinić B, Carrasco L, Gansevoort R, Martino G, Mattace Raso F, Nistor I, Ortiz A, Rastenytė D, Stefan G, Tedeschi G, Bikbov B, Endlich K, Kurganaite J, Perico N, Remuzzi G, Trepiccione F, Blankestijn P, Eckardt K, Fliser D, Gutiérrez-Jiménez E, Konig M, Rychlik I, Deleidi M, Reusz G, Farisco M, Imenez Silva P, Bobot M, Capolongo G. Cognitive disorders in patients with chronic kidney disease: Approaches to prevention and treatment. in European Journal of Neurology. 2023;30(9):2899-2911.
doi:10.1111/ene.15928 .

Pépin, Marion, Klimkowicz-Mrowiec, Aleksandra, Godefroy, Olivier, Delgado, P., Carriazo, S., Ferreira, A.C., Golenia, A., Malyszko, J., Grodzicki, T., Giannakou, K., Paolisso, G., Barbieri, M., Garneata, L., Mocanu, C.A., Liabeuf, S., Spasovski, G., Zoccali, C., Bruchfeld, A., Farinha, A., Arici, M., Capasso, G., Wiecek, A., Massy, Z.A., Andrade, A., Bachmann, M., Bumblyte, I., Covic, A.C., Endlich, N., Engvig, A., Fouque, D., Franssen, C., Frische, S., Gesualdo, L., Goumenos, D., Mani, L.-Y., Marti, H.-P., Mayer, C., Nielsen, R., Pešić, Vesna, Rroji, M., Sakkas, G., Stevens, K., Vazelov, E., Viggiano, D., Zacharia, L., Hoorn, E., Figurek, A., Unwin, R., Wagner, C.A., Wanner, C., Nitsch, D., Fridolin, I., Hafez, G., Soler Romeo, M.J., Batinić, Bojan, Carrasco, L., Gansevoort, R., Martino, G., Mattace Raso, F., Nistor, I., Ortiz, A., Rastenytė, D., Stefan, G., Tedeschi, G., Bikbov, B., Endlich, K.H., Kurganaite, J., Perico, N., Remuzzi, G., Trepiccione, F., Blankestijn, P., Eckardt, K.-U., Fliser, D., Gutiérrez-Jiménez, E., Konig, M., Rychlik, I., Deleidi, M., Reusz, G., Farisco, M., Imenez Silva, P.H., Bobot, M., Capolongo, G., "Cognitive disorders in patients with chronic kidney disease: Approaches to prevention and treatment" in European Journal of Neurology, 30, no. 9 (2023):2899-2911,
https://doi.org/10.1111/ene.15928 . .

TY  - JOUR
AU  - Farisco, Michele
AU  - Zecchino, I.
AU  - Capasso, G.
AU  - Andrade, A.
AU  - Bachmann, M.
AU  - Bumblyte, I.
AU  - Covic, A.C.
AU  - Delgado, P.
AU  - Endlich, N.
AU  - Engvig, A.
AU  - Fouque, D.
AU  - Franssen, C.
AU  - Frische, S.
AU  - Garneata, L.
AU  - Gesualdo, L.
AU  - Giannakou, K.
AU  - Goumenos, D.
AU  - Kartal, A.T.
AU  - Mani, L.-Y.
AU  - Marti, H.-P.
AU  - Mayer, C.
AU  - Nielsen, R.
AU  - Pešić, Vesna
AU  - Rroji, M.
AU  - Sakkas, G.
AU  - Spasovski, G.
AU  - Stevens, K.I.
AU  - Vazelov, E.
AU  - Viggiano, D.
AU  - Zacharia, L.
AU  - Ferreira, A.C.
AU  - Malyszko, J.
AU  - Hoorn, E.
AU  - Figurek, A.
AU  - Unwin, R.
AU  - Wagner, C.
AU  - Wanner, C.
AU  - Bruchfeld, A.
AU  - Pepin, M.
AU  - Wieçek, A.
AU  - Nitsch, D.
AU  - Fridolin, I.
AU  - Hafez, G.
AU  - Soler, M.J.
AU  - Barbieri, M.
AU  - Batinić, Bojan
AU  - Carrasco, L.
AU  - Carriazo, S.
AU  - Gansevoort, R.
AU  - Martino, G.
AU  - Raso, F.M.
AU  - Nistor, I.
AU  - Ortiz, A.
AU  - Paolisso, G.
AU  - Rastenytė, D.
AU  - Stefan, G.
AU  - Tedeschi, G.
AU  - Massy, Z.A.
AU  - Bikbov, B.
AU  - Endlich, K.H.
AU  - Godefroy, O.
AU  - Chillon, J.-M.
AU  - Kossioni, A.
AU  - Kurganaite, J.
AU  - Perico, N.
AU  - Remuzzi, G.
AU  - Grodzicki, T.
AU  - Trepiccione, F.
AU  - Zoccali, C.
AU  - Arici, M.
AU  - Blankestijn, P.
AU  - Eckardt, K.-U.
AU  - Fliser, D.
AU  - Jiménez, E.
AU  - König, M.
AU  - Rychlik, I.
AU  - Deleidi, M.
AU  - Reusz, G.
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5595
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - The need for a multi-disciplinary reflection about frailty and cognitive impairment in chronic kidney disease
VL  - 38
IS  - 5
SP  - 1064
EP  - 1066
DO  - 10.1093/ndt/gfac334
ER  - 

@article{
author = "Farisco, Michele and Zecchino, I. and Capasso, G. and Andrade, A. and Bachmann, M. and Bumblyte, I. and Covic, A.C. and Delgado, P. and Endlich, N. and Engvig, A. and Fouque, D. and Franssen, C. and Frische, S. and Garneata, L. and Gesualdo, L. and Giannakou, K. and Goumenos, D. and Kartal, A.T. and Mani, L.-Y. and Marti, H.-P. and Mayer, C. and Nielsen, R. and Pešić, Vesna and Rroji, M. and Sakkas, G. and Spasovski, G. and Stevens, K.I. and Vazelov, E. and Viggiano, D. and Zacharia, L. and Ferreira, A.C. and Malyszko, J. and Hoorn, E. and Figurek, A. and Unwin, R. and Wagner, C. and Wanner, C. and Bruchfeld, A. and Pepin, M. and Wieçek, A. and Nitsch, D. and Fridolin, I. and Hafez, G. and Soler, M.J. and Barbieri, M. and Batinić, Bojan and Carrasco, L. and Carriazo, S. and Gansevoort, R. and Martino, G. and Raso, F.M. and Nistor, I. and Ortiz, A. and Paolisso, G. and Rastenytė, D. and Stefan, G. and Tedeschi, G. and Massy, Z.A. and Bikbov, B. and Endlich, K.H. and Godefroy, O. and Chillon, J.-M. and Kossioni, A. and Kurganaite, J. and Perico, N. and Remuzzi, G. and Grodzicki, T. and Trepiccione, F. and Zoccali, C. and Arici, M. and Blankestijn, P. and Eckardt, K.-U. and Fliser, D. and Jiménez, E. and König, M. and Rychlik, I. and Deleidi, M. and Reusz, G.",
year = "2023",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "The need for a multi-disciplinary reflection about frailty and cognitive impairment in chronic kidney disease",
volume = "38",
number = "5",
pages = "1064-1066",
doi = "10.1093/ndt/gfac334"
}

Farisco, M., Zecchino, I., Capasso, G., Andrade, A., Bachmann, M., Bumblyte, I., Covic, A.C., Delgado, P., Endlich, N., Engvig, A., Fouque, D., Franssen, C., Frische, S., Garneata, L., Gesualdo, L., Giannakou, K., Goumenos, D., Kartal, A.T., Mani, L.-Y., Marti, H.-P., Mayer, C., Nielsen, R., Pešić, V., Rroji, M., Sakkas, G., Spasovski, G., Stevens, K.I., Vazelov, E., Viggiano, D., Zacharia, L., Ferreira, A.C., Malyszko, J., Hoorn, E., Figurek, A., Unwin, R., Wagner, C., Wanner, C., Bruchfeld, A., Pepin, M., Wieçek, A., Nitsch, D., Fridolin, I., Hafez, G., Soler, M.J., Barbieri, M., Batinić, B., Carrasco, L., Carriazo, S., Gansevoort, R., Martino, G., Raso, F.M., Nistor, I., Ortiz, A., Paolisso, G., Rastenytė, D., Stefan, G., Tedeschi, G., Massy, Z.A., Bikbov, B., Endlich, K.H., Godefroy, O., Chillon, J.-M., Kossioni, A., Kurganaite, J., Perico, N., Remuzzi, G., Grodzicki, T., Trepiccione, F., Zoccali, C., Arici, M., Blankestijn, P., Eckardt, K.-U., Fliser, D., Jiménez, E., König, M., Rychlik, I., Deleidi, M.,& Reusz, G.. (2023). The need for a multi-disciplinary reflection about frailty and cognitive impairment in chronic kidney disease. in Nephrology Dialysis Transplantation
Oxford University Press., 38(5), 1064-1066.
https://doi.org/10.1093/ndt/gfac334

Farisco M, Zecchino I, Capasso G, Andrade A, Bachmann M, Bumblyte I, Covic A, Delgado P, Endlich N, Engvig A, Fouque D, Franssen C, Frische S, Garneata L, Gesualdo L, Giannakou K, Goumenos D, Kartal A, Mani L, Marti H, Mayer C, Nielsen R, Pešić V, Rroji M, Sakkas G, Spasovski G, Stevens K, Vazelov E, Viggiano D, Zacharia L, Ferreira A, Malyszko J, Hoorn E, Figurek A, Unwin R, Wagner C, Wanner C, Bruchfeld A, Pepin M, Wieçek A, Nitsch D, Fridolin I, Hafez G, Soler M, Barbieri M, Batinić B, Carrasco L, Carriazo S, Gansevoort R, Martino G, Raso F, Nistor I, Ortiz A, Paolisso G, Rastenytė D, Stefan G, Tedeschi G, Massy Z, Bikbov B, Endlich K, Godefroy O, Chillon J, Kossioni A, Kurganaite J, Perico N, Remuzzi G, Grodzicki T, Trepiccione F, Zoccali C, Arici M, Blankestijn P, Eckardt K, Fliser D, Jiménez E, König M, Rychlik I, Deleidi M, Reusz G. The need for a multi-disciplinary reflection about frailty and cognitive impairment in chronic kidney disease. in Nephrology Dialysis Transplantation. 2023;38(5):1064-1066.
doi:10.1093/ndt/gfac334 .

Farisco, Michele, Zecchino, I., Capasso, G., Andrade, A., Bachmann, M., Bumblyte, I., Covic, A.C., Delgado, P., Endlich, N., Engvig, A., Fouque, D., Franssen, C., Frische, S., Garneata, L., Gesualdo, L., Giannakou, K., Goumenos, D., Kartal, A.T., Mani, L.-Y., Marti, H.-P., Mayer, C., Nielsen, R., Pešić, Vesna, Rroji, M., Sakkas, G., Spasovski, G., Stevens, K.I., Vazelov, E., Viggiano, D., Zacharia, L., Ferreira, A.C., Malyszko, J., Hoorn, E., Figurek, A., Unwin, R., Wagner, C., Wanner, C., Bruchfeld, A., Pepin, M., Wieçek, A., Nitsch, D., Fridolin, I., Hafez, G., Soler, M.J., Barbieri, M., Batinić, Bojan, Carrasco, L., Carriazo, S., Gansevoort, R., Martino, G., Raso, F.M., Nistor, I., Ortiz, A., Paolisso, G., Rastenytė, D., Stefan, G., Tedeschi, G., Massy, Z.A., Bikbov, B., Endlich, K.H., Godefroy, O., Chillon, J.-M., Kossioni, A., Kurganaite, J., Perico, N., Remuzzi, G., Grodzicki, T., Trepiccione, F., Zoccali, C., Arici, M., Blankestijn, P., Eckardt, K.-U., Fliser, D., Jiménez, E., König, M., Rychlik, I., Deleidi, M., Reusz, G., "The need for a multi-disciplinary reflection about frailty and cognitive impairment in chronic kidney disease" in Nephrology Dialysis Transplantation, 38, no. 5 (2023):1064-1066,
https://doi.org/10.1093/ndt/gfac334 . .

TY  - JOUR
AU  - Milosavljević, Filip
AU  - Brusini, Irene
AU  - Atanasov, Andrea
AU  - Manojlović, Marina
AU  - Vučić, Marija
AU  - Oreščanin-Dušić, Zorana
AU  - Brkljačić, Jelena
AU  - Miljević, Čedo
AU  - Nikolić-Kokić, Aleksandra
AU  - Blagojević, Duško
AU  - Wang, Chunliang
AU  - Damberg, Peter
AU  - Pešić, Vesna
AU  - Tyndale, Rachel F.
AU  - Ingelman-Sundberg, Magnus
AU  - Jukić, Marin
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4516
AB  - Aims: CYP2C19 transgenic mouse expresses the human CYP2C19 gene in the liver and developing brain, and it exhibits altered neurodevelopment associated with impairments in emotionality and locomotion. Because the validation of new animal models is essential for the understanding of the aetiology and pathophysiology of movement disorders, the objective was to characterise motoric phenotype in CYP2C19 transgenic mice and to investigate its validity as a new animal model of ataxia. Methods: The rotarod, paw-print and beam-walking tests were utilised to characterise the motoric phenotype. The volumes of 20 brain regions in CYP2C19 transgenic and wild-type mice were quantified by 9.4T gadolinium-enhanced post-mortem structural neuroimaging. Antioxidative enzymatic activity was quantified biochemically. Dopaminergic alterations were characterised by chromatographic quantification of concentrations of dopamine and its metabolites and by subsequent immunohistochemical analyses. The beam-walking test was repeated after the treatment with dopamine receptor antagonists ecopipam and raclopride. Results: CYP2C19 transgenic mice exhibit abnormal, unilateral ataxia-like gait, clasping reflex and 5.6-fold more paw-slips in the beam-walking test; the motoric phenotype was more pronounced in youth. Transgenic mice exhibited a profound reduction of 12% in cerebellar volume and a moderate reduction of 4% in hippocampal volume; both regions exhibited an increased antioxidative enzyme activity. CYP2C19 mice were hyperdopaminergic; however, the motoric impairment was not ameliorated by dopamine receptor antagonists, and there was no alteration in the number of midbrain dopaminergic neurons in CYP2C19 mice. Conclusions: Humanised CYP2C19 transgenic mice exhibit altered gait and functional motoric impairments; this phenotype is likely caused by an aberrant cerebellar development.
PB  - John Wiley and Sons Inc
T2  - Neuropathology and Applied Neurobiology
T1  - The humanised CYP2C19 transgenic mouse exhibits cerebellar atrophy and movement impairment reminiscent of ataxia
VL  - 49
IS  - 1
DO  - 10.1111/nan.12867
ER  - 

@article{
author = "Milosavljević, Filip and Brusini, Irene and Atanasov, Andrea and Manojlović, Marina and Vučić, Marija and Oreščanin-Dušić, Zorana and Brkljačić, Jelena and Miljević, Čedo and Nikolić-Kokić, Aleksandra and Blagojević, Duško and Wang, Chunliang and Damberg, Peter and Pešić, Vesna and Tyndale, Rachel F. and Ingelman-Sundberg, Magnus and Jukić, Marin",
year = "2023",
abstract = "Aims: CYP2C19 transgenic mouse expresses the human CYP2C19 gene in the liver and developing brain, and it exhibits altered neurodevelopment associated with impairments in emotionality and locomotion. Because the validation of new animal models is essential for the understanding of the aetiology and pathophysiology of movement disorders, the objective was to characterise motoric phenotype in CYP2C19 transgenic mice and to investigate its validity as a new animal model of ataxia. Methods: The rotarod, paw-print and beam-walking tests were utilised to characterise the motoric phenotype. The volumes of 20 brain regions in CYP2C19 transgenic and wild-type mice were quantified by 9.4T gadolinium-enhanced post-mortem structural neuroimaging. Antioxidative enzymatic activity was quantified biochemically. Dopaminergic alterations were characterised by chromatographic quantification of concentrations of dopamine and its metabolites and by subsequent immunohistochemical analyses. The beam-walking test was repeated after the treatment with dopamine receptor antagonists ecopipam and raclopride. Results: CYP2C19 transgenic mice exhibit abnormal, unilateral ataxia-like gait, clasping reflex and 5.6-fold more paw-slips in the beam-walking test; the motoric phenotype was more pronounced in youth. Transgenic mice exhibited a profound reduction of 12% in cerebellar volume and a moderate reduction of 4% in hippocampal volume; both regions exhibited an increased antioxidative enzyme activity. CYP2C19 mice were hyperdopaminergic; however, the motoric impairment was not ameliorated by dopamine receptor antagonists, and there was no alteration in the number of midbrain dopaminergic neurons in CYP2C19 mice. Conclusions: Humanised CYP2C19 transgenic mice exhibit altered gait and functional motoric impairments; this phenotype is likely caused by an aberrant cerebellar development.",
publisher = "John Wiley and Sons Inc",
journal = "Neuropathology and Applied Neurobiology",
title = "The humanised CYP2C19 transgenic mouse exhibits cerebellar atrophy and movement impairment reminiscent of ataxia",
volume = "49",
number = "1",
doi = "10.1111/nan.12867"
}

Milosavljević, F., Brusini, I., Atanasov, A., Manojlović, M., Vučić, M., Oreščanin-Dušić, Z., Brkljačić, J., Miljević, Č., Nikolić-Kokić, A., Blagojević, D., Wang, C., Damberg, P., Pešić, V., Tyndale, R. F., Ingelman-Sundberg, M.,& Jukić, M.. (2023). The humanised CYP2C19 transgenic mouse exhibits cerebellar atrophy and movement impairment reminiscent of ataxia. in Neuropathology and Applied Neurobiology
John Wiley and Sons Inc., 49(1).
https://doi.org/10.1111/nan.12867

Milosavljević F, Brusini I, Atanasov A, Manojlović M, Vučić M, Oreščanin-Dušić Z, Brkljačić J, Miljević Č, Nikolić-Kokić A, Blagojević D, Wang C, Damberg P, Pešić V, Tyndale RF, Ingelman-Sundberg M, Jukić M. The humanised CYP2C19 transgenic mouse exhibits cerebellar atrophy and movement impairment reminiscent of ataxia. in Neuropathology and Applied Neurobiology. 2023;49(1).
doi:10.1111/nan.12867 .

Milosavljević, Filip, Brusini, Irene, Atanasov, Andrea, Manojlović, Marina, Vučić, Marija, Oreščanin-Dušić, Zorana, Brkljačić, Jelena, Miljević, Čedo, Nikolić-Kokić, Aleksandra, Blagojević, Duško, Wang, Chunliang, Damberg, Peter, Pešić, Vesna, Tyndale, Rachel F., Ingelman-Sundberg, Magnus, Jukić, Marin, "The humanised CYP2C19 transgenic mouse exhibits cerebellar atrophy and movement impairment reminiscent of ataxia" in Neuropathology and Applied Neurobiology, 49, no. 1 (2023),
https://doi.org/10.1111/nan.12867 . .

TY  - JOUR
AU  - Liabeuf, Sophie
AU  - Pešić, Vesna
AU  - Spasovski, Goce
AU  - Maciulaitis, Romaldas
AU  - Bobot, Mickaël
AU  - Farinha, Ana
AU  - Wagner, Carsten A.
AU  - Unwin, Robert J.
AU  - Capasso, Giovambattista
AU  - Bumblyte, Inga Arune
AU  - Hafez, Gaye
PY  - 2023
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5225
AB  - People living with chronic kidney disease (CKD) frequently suffer from mild cognitive impairment and/or other
neurocognitive disorders. This review in two parts will focus on adverse drug reactions resulting in cognitive impairment
as a potentially modifiable risk factor in CKD patients. Many patients with CKD have a substantial burden of
comorbidities leading to polypharmacy. A recent study found that patients seen by nephrologists were the most complex
to treat because of their high number of comorbidities and medications. Due to polypharmacy, these patients may
experience a wide range of adverse drug reactions. Along with CKD progression, the accumulation of uremic toxins may
lead to blood–brain barrier (BBB) disruption and pharmacokinetic alterations, increasing the risk of adverse reactions
affecting the central nervous system (CNS). In patients on dialysis, the excretion of drugs that depend on kidney
function is severely reduced such that adverse and toxic levels of a drug or its metabolites may be reached at relatively
low doses, unless dosing is adjusted. This first review will discuss how CKD represents a risk factor for adverse drug
reactions affecting the CNS via (i) BBB disruption associated with CKD and (ii) the impact of reduced kidney function and
dialysis itself on drug pharmacokinetics.
PB  - Oxford University Press ( Oxford Academic)
T2  - Clinical Kidney Journal
T1  - Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor
VL  - 0
IS  - 0
SP  - 1
EP  - 13
DO  - 10.1093/ckj/sfad241
ER  - 

@article{
author = "Liabeuf, Sophie and Pešić, Vesna and Spasovski, Goce and Maciulaitis, Romaldas and Bobot, Mickaël and Farinha, Ana and Wagner, Carsten A. and Unwin, Robert J. and Capasso, Giovambattista and Bumblyte, Inga Arune and Hafez, Gaye",
year = "2023",
abstract = "People living with chronic kidney disease (CKD) frequently suffer from mild cognitive impairment and/or other
neurocognitive disorders. This review in two parts will focus on adverse drug reactions resulting in cognitive impairment
as a potentially modifiable risk factor in CKD patients. Many patients with CKD have a substantial burden of
comorbidities leading to polypharmacy. A recent study found that patients seen by nephrologists were the most complex
to treat because of their high number of comorbidities and medications. Due to polypharmacy, these patients may
experience a wide range of adverse drug reactions. Along with CKD progression, the accumulation of uremic toxins may
lead to blood–brain barrier (BBB) disruption and pharmacokinetic alterations, increasing the risk of adverse reactions
affecting the central nervous system (CNS). In patients on dialysis, the excretion of drugs that depend on kidney
function is severely reduced such that adverse and toxic levels of a drug or its metabolites may be reached at relatively
low doses, unless dosing is adjusted. This first review will discuss how CKD represents a risk factor for adverse drug
reactions affecting the CNS via (i) BBB disruption associated with CKD and (ii) the impact of reduced kidney function and
dialysis itself on drug pharmacokinetics.",
publisher = "Oxford University Press ( Oxford Academic)",
journal = "Clinical Kidney Journal",
title = "Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor",
volume = "0",
number = "0",
pages = "1-13",
doi = "10.1093/ckj/sfad241"
}

Liabeuf, S., Pešić, V., Spasovski, G., Maciulaitis, R., Bobot, M., Farinha, A., Wagner, C. A., Unwin, R. J., Capasso, G., Bumblyte, I. A.,& Hafez, G.. (2023). Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor. in Clinical Kidney Journal
Oxford University Press ( Oxford Academic)., 0(0), 1-13.
https://doi.org/10.1093/ckj/sfad241

Liabeuf S, Pešić V, Spasovski G, Maciulaitis R, Bobot M, Farinha A, Wagner CA, Unwin RJ, Capasso G, Bumblyte IA, Hafez G. Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor. in Clinical Kidney Journal. 2023;0(0):1-13.
doi:10.1093/ckj/sfad241 .

Liabeuf, Sophie, Pešić, Vesna, Spasovski, Goce, Maciulaitis, Romaldas, Bobot, Mickaël, Farinha, Ana, Wagner, Carsten A., Unwin, Robert J., Capasso, Giovambattista, Bumblyte, Inga Arune, Hafez, Gaye, "Drugs with a negative impact on cognitive function (Part 1): chronic kidney disease as a risk factor" in Clinical Kidney Journal, 0, no. 0 (2023):1-13,
https://doi.org/10.1093/ckj/sfad241 . .

TY  - JOUR
AU  - Bikbov, Boris
AU  - Soler, Maria Jose ́
AU  - Pešić, Vesna
AU  - Capasso, Giovambattista
AU  - Unwin, Robert
AU  - Endres, Matthias
AU  - Remuzzi, Giuseppe
AU  - Perico, Norberto
AU  - Gansevoort, Ron
AU  - Mattace-Raso, Francesco
AU  - Bruchfeld, Annette
AU  - Figurek, Andreja
AU  - Hafez, Gaye
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4031
AB  - Kidney dysfunction can profoundly influence many organ systems, and recent evidence suggests a potential role for increased albuminuria in the development of mild cognitive impairment (MCI) or dementia. Epidemiological studies conducted in different populations have demonstrated that the presence of increased albuminuria is associated with a higher relative risk of MCI or dementia both in cross-sectional analyses and in studies with long-term follow-up. The underlying pathophysiological mechanisms of albuminuria's effect are as yet insufficiently studied, with several important knowledge gaps still present in a complex relationship with other MCI and dementia risk factors. Both the kidney and the brain have microvascular similarities that make them sensitive to endothelial dysfunction involving different mechanisms, including oxidative stress and inflammation. The exact substrate of MCI and dementia is still under investigation, however available experimental data indicate that elevated albuminuria and low glomerular filtration rate are associated with significant neuroanatomical declines in hippocampal function and grey matter volume. Thus, albuminuria may be critical in the development of cognitive impairment and its progression to dementia. In this review, we summarize the available evidence on albuminuria's link to MCI and dementia, point to existing gaps in our knowledge and suggest actions to overcome them. The major question of whether interventions that target increased albuminuria could prevent cognitive decline remains unanswered. Our recommendations for future research are aimed at helping to plan clinical trials and to solve the complex conundrum outlined in this review, with the ultimate goal of improving the lives of patients with chronic kidney disease.
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?
VL  - 37
IS  - supplement 2
SP  - ii55
EP  - ii62
DO  - 10.1093/ndt/gfab261
ER  - 

@article{
author = "Bikbov, Boris and Soler, Maria Jose ́ and Pešić, Vesna and Capasso, Giovambattista and Unwin, Robert and Endres, Matthias and Remuzzi, Giuseppe and Perico, Norberto and Gansevoort, Ron and Mattace-Raso, Francesco and Bruchfeld, Annette and Figurek, Andreja and Hafez, Gaye",
year = "2022",
abstract = "Kidney dysfunction can profoundly influence many organ systems, and recent evidence suggests a potential role for increased albuminuria in the development of mild cognitive impairment (MCI) or dementia. Epidemiological studies conducted in different populations have demonstrated that the presence of increased albuminuria is associated with a higher relative risk of MCI or dementia both in cross-sectional analyses and in studies with long-term follow-up. The underlying pathophysiological mechanisms of albuminuria's effect are as yet insufficiently studied, with several important knowledge gaps still present in a complex relationship with other MCI and dementia risk factors. Both the kidney and the brain have microvascular similarities that make them sensitive to endothelial dysfunction involving different mechanisms, including oxidative stress and inflammation. The exact substrate of MCI and dementia is still under investigation, however available experimental data indicate that elevated albuminuria and low glomerular filtration rate are associated with significant neuroanatomical declines in hippocampal function and grey matter volume. Thus, albuminuria may be critical in the development of cognitive impairment and its progression to dementia. In this review, we summarize the available evidence on albuminuria's link to MCI and dementia, point to existing gaps in our knowledge and suggest actions to overcome them. The major question of whether interventions that target increased albuminuria could prevent cognitive decline remains unanswered. Our recommendations for future research are aimed at helping to plan clinical trials and to solve the complex conundrum outlined in this review, with the ultimate goal of improving the lives of patients with chronic kidney disease.",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?",
volume = "37",
number = "supplement 2",
pages = "ii55-ii62",
doi = "10.1093/ndt/gfab261"
}

Bikbov, B., Soler, M. J. ́., Pešić, V., Capasso, G., Unwin, R., Endres, M., Remuzzi, G., Perico, N., Gansevoort, R., Mattace-Raso, F., Bruchfeld, A., Figurek, A.,& Hafez, G.. (2022). Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?. in Nephrology Dialysis Transplantation
Oxford University Press., 37(supplement 2), ii55-ii62.
https://doi.org/10.1093/ndt/gfab261

Bikbov B, Soler MJ́, Pešić V, Capasso G, Unwin R, Endres M, Remuzzi G, Perico N, Gansevoort R, Mattace-Raso F, Bruchfeld A, Figurek A, Hafez G. Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?. in Nephrology Dialysis Transplantation. 2022;37(supplement 2):ii55-ii62.
doi:10.1093/ndt/gfab261 .

Bikbov, Boris, Soler, Maria Jose ́, Pešić, Vesna, Capasso, Giovambattista, Unwin, Robert, Endres, Matthias, Remuzzi, Giuseppe, Perico, Norberto, Gansevoort, Ron, Mattace-Raso, Francesco, Bruchfeld, Annette, Figurek, Andreja, Hafez, Gaye, "Albuminuria as a risk factor for mild cognitive impairment and dementia-what is the evidence?" in Nephrology Dialysis Transplantation, 37, no. supplement 2 (2022):ii55-ii62,
https://doi.org/10.1093/ndt/gfab261 . .

TY  - JOUR
AU  - Viggiano, Davide
AU  - Bruchfeld, Annette
AU  - Carriazo, Sol
AU  - de Donato, Antonio
AU  - Endlich, Nicole
AU  - Ferreira, Ana Carina
AU  - Figurek, Andreja
AU  - Fouque, Denis
AU  - Franssen, Casper F.M.
AU  - Giannakou, Konstantinos
AU  - Goumenos, Dimitrios
AU  - Hoorn, Ewout J.
AU  - Nitsch, Dorothea
AU  - Ortiz, Alberto
AU  - Pešić, Vesna
AU  - Rastenyté, Daiva
AU  - Soler, Maria José
AU  - Rroji, Merita
AU  - Trepiccione, Francesco
AU  - Unwin, Robert J.
AU  - Wagner, Carsten A.
AU  - Wieçek, Andrzej
AU  - Zacchia, Miriam
AU  - Zoccali, Carmine
AU  - Capasso, Giovambattista
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4030
AB  - Kidney function has two important elements: glomerular filtration and tubular function (secretion and reabsorption). A persistent decrease in glomerular filtration rate (GFR), with or without proteinuria, is diagnostic of chronic kidney disease (CKD). While glomerular injury or disease is a major cause of CKD and usually associated with proteinuria, predominant tubular injury, with or without tubulointerstitial disease, is typically non-proteinuric. CKD has been linked with cognitive impairment, but it is unclear how much this depends on a decreased GFR, altered tubular function or the presence of proteinuria. Since CKD is often accompanied by tubular and interstitial dysfunction, we explore here for the first time the potential role of the tubular and tubulointerstitial compartments in cognitive dysfunction. To help address this issue we selected a group of primary tubular diseases with preserved GFR in which to review the evidence for any association with brain dysfunction. Cognition, mood, neurosensory and motor disturbances are not well characterized in tubular diseases, possibly because they are subclinical and less prominent than other clinical manifestations. The available literature suggests that brain dysfunction in tubular and tubulointerstitial diseases is usually mild and is more often seen in disorders of water handling. Brain dysfunction may occur when severe electrolyte and water disorders in young children persist over a long period of time before the diagnosis is made. We have chosen Bartter and Gitelman syndromes and nephrogenic diabetes insipidus as examples to highlight this topic. We discuss current published findings, some unanswered questions and propose topics for future research.
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - Brain dysfunction in tubular and tubulointerstitial kidney diseases
VL  - 37
IS  - supplement 2
SP  - ii46
EP  - ii55
DO  - 10.1093/ndt/gfab276
ER  - 

@article{
author = "Viggiano, Davide and Bruchfeld, Annette and Carriazo, Sol and de Donato, Antonio and Endlich, Nicole and Ferreira, Ana Carina and Figurek, Andreja and Fouque, Denis and Franssen, Casper F.M. and Giannakou, Konstantinos and Goumenos, Dimitrios and Hoorn, Ewout J. and Nitsch, Dorothea and Ortiz, Alberto and Pešić, Vesna and Rastenyté, Daiva and Soler, Maria José and Rroji, Merita and Trepiccione, Francesco and Unwin, Robert J. and Wagner, Carsten A. and Wieçek, Andrzej and Zacchia, Miriam and Zoccali, Carmine and Capasso, Giovambattista",
year = "2022",
abstract = "Kidney function has two important elements: glomerular filtration and tubular function (secretion and reabsorption). A persistent decrease in glomerular filtration rate (GFR), with or without proteinuria, is diagnostic of chronic kidney disease (CKD). While glomerular injury or disease is a major cause of CKD and usually associated with proteinuria, predominant tubular injury, with or without tubulointerstitial disease, is typically non-proteinuric. CKD has been linked with cognitive impairment, but it is unclear how much this depends on a decreased GFR, altered tubular function or the presence of proteinuria. Since CKD is often accompanied by tubular and interstitial dysfunction, we explore here for the first time the potential role of the tubular and tubulointerstitial compartments in cognitive dysfunction. To help address this issue we selected a group of primary tubular diseases with preserved GFR in which to review the evidence for any association with brain dysfunction. Cognition, mood, neurosensory and motor disturbances are not well characterized in tubular diseases, possibly because they are subclinical and less prominent than other clinical manifestations. The available literature suggests that brain dysfunction in tubular and tubulointerstitial diseases is usually mild and is more often seen in disorders of water handling. Brain dysfunction may occur when severe electrolyte and water disorders in young children persist over a long period of time before the diagnosis is made. We have chosen Bartter and Gitelman syndromes and nephrogenic diabetes insipidus as examples to highlight this topic. We discuss current published findings, some unanswered questions and propose topics for future research.",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "Brain dysfunction in tubular and tubulointerstitial kidney diseases",
volume = "37",
number = "supplement 2",
pages = "ii46-ii55",
doi = "10.1093/ndt/gfab276"
}

Viggiano, D., Bruchfeld, A., Carriazo, S., de Donato, A., Endlich, N., Ferreira, A. C., Figurek, A., Fouque, D., Franssen, C. F.M., Giannakou, K., Goumenos, D., Hoorn, E. J., Nitsch, D., Ortiz, A., Pešić, V., Rastenyté, D., Soler, M. J., Rroji, M., Trepiccione, F., Unwin, R. J., Wagner, C. A., Wieçek, A., Zacchia, M., Zoccali, C.,& Capasso, G.. (2022). Brain dysfunction in tubular and tubulointerstitial kidney diseases. in Nephrology Dialysis Transplantation
Oxford University Press., 37(supplement 2), ii46-ii55.
https://doi.org/10.1093/ndt/gfab276

Viggiano D, Bruchfeld A, Carriazo S, de Donato A, Endlich N, Ferreira AC, Figurek A, Fouque D, Franssen CF, Giannakou K, Goumenos D, Hoorn EJ, Nitsch D, Ortiz A, Pešić V, Rastenyté D, Soler MJ, Rroji M, Trepiccione F, Unwin RJ, Wagner CA, Wieçek A, Zacchia M, Zoccali C, Capasso G. Brain dysfunction in tubular and tubulointerstitial kidney diseases. in Nephrology Dialysis Transplantation. 2022;37(supplement 2):ii46-ii55.
doi:10.1093/ndt/gfab276 .

Viggiano, Davide, Bruchfeld, Annette, Carriazo, Sol, de Donato, Antonio, Endlich, Nicole, Ferreira, Ana Carina, Figurek, Andreja, Fouque, Denis, Franssen, Casper F.M., Giannakou, Konstantinos, Goumenos, Dimitrios, Hoorn, Ewout J., Nitsch, Dorothea, Ortiz, Alberto, Pešić, Vesna, Rastenyté, Daiva, Soler, Maria José, Rroji, Merita, Trepiccione, Francesco, Unwin, Robert J., Wagner, Carsten A., Wieçek, Andrzej, Zacchia, Miriam, Zoccali, Carmine, Capasso, Giovambattista, "Brain dysfunction in tubular and tubulointerstitial kidney diseases" in Nephrology Dialysis Transplantation, 37, no. supplement 2 (2022):ii46-ii55,
https://doi.org/10.1093/ndt/gfab276 . .

TY  - JOUR
AU  - Liabeuf, Sophie
AU  - Pepin, , Marion
AU  - Franssen, Casper F.M.
AU  - Viggiano, Davide
AU  - Carriazo, Sol
AU  - Gansevoort, Ron T.
AU  - Gesualdo, Loreto
AU  - Hafez, Gaye
AU  - Malyszko, Jolanta
AU  - Mayer, Christopher
AU  - Nitsch, Dorothea
AU  - Ortiz, Alberto
AU  - Pešić, Vesna
AU  - Wiecek, Andrzej
AU  - Massy, Ziad
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4029
AB  - Chronic kidney disease (CKD) perturbs the crosstalk with others organs, with the interaction between the kidneys and the heart having been studied most intensively. However, a growing body of data indicates that there is an association between kidney dysfunction and disorders of the central nervous system. In epidemiological studies, CKD is associated with a high prevalence of neurological complications, such as cerebrovascular disorders, movement disorders, cognitive impairment and depression. Along with traditional cardiovascular risk factors (such as diabetes, inflammation, hypertension and dyslipidaemia), non-traditional risk factors related to kidney damage (such as uraemic toxins) may predispose patients with CKD to neurological disorders. There is increasing evidence to show that uraemic toxins, for example indoxyl sulphate, have a neurotoxic effect. A better understanding of factors responsible for the elevated prevalence of neurological disorders among patients with CKD might facilitate the development of novel treatments. Here, we review (i) the potential clinical impact of CKD on cerebrovascular and neurological complications, (ii) the mechanisms underlying the uraemic toxins' putative action (based on pre-clinical and clinical research) and (iii) the potential impact of these findings on patient care.
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?
VL  - 37
IS  - supplement 2
SP  - ii33
EP  - ii44
DO  - 10.1093/ndt/gfab223
ER  - 

@article{
author = "Liabeuf, Sophie and Pepin, , Marion and Franssen, Casper F.M. and Viggiano, Davide and Carriazo, Sol and Gansevoort, Ron T. and Gesualdo, Loreto and Hafez, Gaye and Malyszko, Jolanta and Mayer, Christopher and Nitsch, Dorothea and Ortiz, Alberto and Pešić, Vesna and Wiecek, Andrzej and Massy, Ziad",
year = "2022",
abstract = "Chronic kidney disease (CKD) perturbs the crosstalk with others organs, with the interaction between the kidneys and the heart having been studied most intensively. However, a growing body of data indicates that there is an association between kidney dysfunction and disorders of the central nervous system. In epidemiological studies, CKD is associated with a high prevalence of neurological complications, such as cerebrovascular disorders, movement disorders, cognitive impairment and depression. Along with traditional cardiovascular risk factors (such as diabetes, inflammation, hypertension and dyslipidaemia), non-traditional risk factors related to kidney damage (such as uraemic toxins) may predispose patients with CKD to neurological disorders. There is increasing evidence to show that uraemic toxins, for example indoxyl sulphate, have a neurotoxic effect. A better understanding of factors responsible for the elevated prevalence of neurological disorders among patients with CKD might facilitate the development of novel treatments. Here, we review (i) the potential clinical impact of CKD on cerebrovascular and neurological complications, (ii) the mechanisms underlying the uraemic toxins' putative action (based on pre-clinical and clinical research) and (iii) the potential impact of these findings on patient care.",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?",
volume = "37",
number = "supplement 2",
pages = "ii33-ii44",
doi = "10.1093/ndt/gfab223"
}

Liabeuf, S., Pepin, ,. M., Franssen, C. F.M., Viggiano, D., Carriazo, S., Gansevoort, R. T., Gesualdo, L., Hafez, G., Malyszko, J., Mayer, C., Nitsch, D., Ortiz, A., Pešić, V., Wiecek, A.,& Massy, Z.. (2022). Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?. in Nephrology Dialysis Transplantation
Oxford University Press., 37(supplement 2), ii33-ii44.
https://doi.org/10.1093/ndt/gfab223

Liabeuf S, Pepin ,M, Franssen CF, Viggiano D, Carriazo S, Gansevoort RT, Gesualdo L, Hafez G, Malyszko J, Mayer C, Nitsch D, Ortiz A, Pešić V, Wiecek A, Massy Z. Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?. in Nephrology Dialysis Transplantation. 2022;37(supplement 2):ii33-ii44.
doi:10.1093/ndt/gfab223 .

Liabeuf, Sophie, Pepin, , Marion, Franssen, Casper F.M., Viggiano, Davide, Carriazo, Sol, Gansevoort, Ron T., Gesualdo, Loreto, Hafez, Gaye, Malyszko, Jolanta, Mayer, Christopher, Nitsch, Dorothea, Ortiz, Alberto, Pešić, Vesna, Wiecek, Andrzej, Massy, Ziad, "Chronic kidney disease and neurological disorders: are uraemic toxins the missing piece of the puzzle?" in Nephrology Dialysis Transplantation, 37, no. supplement 2 (2022):ii33-ii44,
https://doi.org/10.1093/ndt/gfab223 . .

TY  - JOUR
AU  - Imenez Silva, Pedro H.
AU  - Unwin, Robert
AU  - Hoorn, Ewout J.
AU  - Ortiz, Alberto
AU  - Trepiccione, Francesco
AU  - Nielsen, Rikke
AU  - Pešić, Vesna
AU  - Hafez, Gaye
AU  - Fouque, , Denis
AU  - Massy, Ziad A.
AU  - De Zeeuw, Chris I.
AU  - Capasso, Giovambattist
AU  - Wagner, Carsten
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4028
AB  - Metabolic acidosis, defined as a plasma or serum bicarbonate concentration <22 mmol/L, is a frequent consequence of chronic kidney disease (CKD) and occurs in ~10-30% of patients with advanced stages of CKD. Likewise, in patients with a kidney transplant, prevalence rates of metabolic acidosis range from 20% to 50%. CKD has recently been associated with cognitive dysfunction, including mild cognitive impairment with memory and attention deficits, reduced executive functions and morphological damage detectable with imaging. Also, impaired motor functions and loss of muscle strength are often found in patients with advanced CKD, which in part may be attributed to altered central nervous system (CNS) functions. While the exact mechanisms of how CKD may cause cognitive dysfunction and reduced motor functions are still debated, recent data point towards the possibility that acidosis is one modifiable contributor to cognitive dysfunction. This review summarizes recent evidence for an association between acidosis and cognitive dysfunction in patients with CKD and discusses potential mechanisms by which acidosis may impact CNS functions. The review also identifies important open questions to be answered to improve prevention and therapy of cognitive dysfunction in the setting of metabolic acidosis in patients with CKD.
PB  - Oxford University Press
T2  - Nephrology Dialysis Transplantation
T1  - Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease
VL  - 37
IS  - supplement 2
SP  - ii4
EP  - ii12
DO  - 10.1093/ndt/gfab216
ER  - 

@article{
author = "Imenez Silva, Pedro H. and Unwin, Robert and Hoorn, Ewout J. and Ortiz, Alberto and Trepiccione, Francesco and Nielsen, Rikke and Pešić, Vesna and Hafez, Gaye and Fouque, , Denis and Massy, Ziad A. and De Zeeuw, Chris I. and Capasso, Giovambattist and Wagner, Carsten",
year = "2022",
abstract = "Metabolic acidosis, defined as a plasma or serum bicarbonate concentration <22 mmol/L, is a frequent consequence of chronic kidney disease (CKD) and occurs in ~10-30% of patients with advanced stages of CKD. Likewise, in patients with a kidney transplant, prevalence rates of metabolic acidosis range from 20% to 50%. CKD has recently been associated with cognitive dysfunction, including mild cognitive impairment with memory and attention deficits, reduced executive functions and morphological damage detectable with imaging. Also, impaired motor functions and loss of muscle strength are often found in patients with advanced CKD, which in part may be attributed to altered central nervous system (CNS) functions. While the exact mechanisms of how CKD may cause cognitive dysfunction and reduced motor functions are still debated, recent data point towards the possibility that acidosis is one modifiable contributor to cognitive dysfunction. This review summarizes recent evidence for an association between acidosis and cognitive dysfunction in patients with CKD and discusses potential mechanisms by which acidosis may impact CNS functions. The review also identifies important open questions to be answered to improve prevention and therapy of cognitive dysfunction in the setting of metabolic acidosis in patients with CKD.",
publisher = "Oxford University Press",
journal = "Nephrology Dialysis Transplantation",
title = "Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease",
volume = "37",
number = "supplement 2",
pages = "ii4-ii12",
doi = "10.1093/ndt/gfab216"
}

Imenez Silva, P. H., Unwin, R., Hoorn, E. J., Ortiz, A., Trepiccione, F., Nielsen, R., Pešić, V., Hafez, G., Fouque, ,. D., Massy, Z. A., De Zeeuw, C. I., Capasso, G.,& Wagner, C.. (2022). Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease. in Nephrology Dialysis Transplantation
Oxford University Press., 37(supplement 2), ii4-ii12.
https://doi.org/10.1093/ndt/gfab216

Imenez Silva PH, Unwin R, Hoorn EJ, Ortiz A, Trepiccione F, Nielsen R, Pešić V, Hafez G, Fouque ,D, Massy ZA, De Zeeuw CI, Capasso G, Wagner C. Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease. in Nephrology Dialysis Transplantation. 2022;37(supplement 2):ii4-ii12.
doi:10.1093/ndt/gfab216 .

Imenez Silva, Pedro H., Unwin, Robert, Hoorn, Ewout J., Ortiz, Alberto, Trepiccione, Francesco, Nielsen, Rikke, Pešić, Vesna, Hafez, Gaye, Fouque, , Denis, Massy, Ziad A., De Zeeuw, Chris I., Capasso, Giovambattist, Wagner, Carsten, "Acidosis, cognitive dysfunction and motor impairments in patients with kidney disease" in Nephrology Dialysis Transplantation, 37, no. supplement 2 (2022):ii4-ii12,
https://doi.org/10.1093/ndt/gfab216 . .

TY  - CONF
AU  - Pejušković, Bojana
AU  - Lero, M.
AU  - Đekić, J.
AU  - Nikolašević, Gorana
AU  - Dobrosavljević, Ana
AU  - Petrović, Jelena
AU  - Pešić, Vesna
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4364
AB  - Depression causes immense burden on health care systems worldwide with two time s higher prevalence in women. However, both male and female patients are treated with antidepressants under same protocols. As it was demonstrated that estrogen has a prodepressant and testosterone an antidepressant affect, it is reasonable to assume that pharmacotherapeutic effect might depend also on sex hormones status. The aim of this pilot study was to explore hormonal status of female and male patients upon hospitalization on occurrence of depressive episode and to correlate it with pharmacotherapy effect after four weeks of therapy. Subjects were 42 patients, 14 males, 14 females in the first (follicular) phase of menstrual cycle and 14 females in the second (luteal) phase of menstrual cycle upon hospitalization. The Hamilton scale was used to determine degree of depressive state upon hospitalization an after 28 days. At both time points, blood was sampled and level of testosterone and estrogen for male and estrogen, progesterone and testosterone for female patients was analysed. Results of the study showed that antidepressant effect calculated as a difference in Hamilton scale was highest in male group of patients and significantly higher than in women in the second phase of the cycle (10.4 vs 8.1). This correlated with increase of testosterone in male patients during four weeks treatment (12.08 vs. 9.46), while there was no significant change in the level of testosterone in both female groups of patients. Furthermore, in female patients in the luteal phase of the cycle, with lowest response to antidepressants, both estrogen and progesterone were significantly reduced during four weeks of treatment. In conclusion, results of our pilot study suggest sex differences in response to antidepressant therapy and level of hormonal status should be evaluated for better personalized pharmacotherapy.
PB  - John Wiley & Sons, Inc
C3  - FEBS Open Bio
T1  - Sex steroid hormones status influence on
antidepressant pharmacotherapy effect in
male and female patients
VL  - 12
IS  - S1
SP  - 325
EP  - 325
DO  - 10.1002/2211-5463.13440
ER  - 

@conference{
author = "Pejušković, Bojana and Lero, M. and Đekić, J. and Nikolašević, Gorana and Dobrosavljević, Ana and Petrović, Jelena and Pešić, Vesna",
year = "2022",
abstract = "Depression causes immense burden on health care systems worldwide with two time s higher prevalence in women. However, both male and female patients are treated with antidepressants under same protocols. As it was demonstrated that estrogen has a prodepressant and testosterone an antidepressant affect, it is reasonable to assume that pharmacotherapeutic effect might depend also on sex hormones status. The aim of this pilot study was to explore hormonal status of female and male patients upon hospitalization on occurrence of depressive episode and to correlate it with pharmacotherapy effect after four weeks of therapy. Subjects were 42 patients, 14 males, 14 females in the first (follicular) phase of menstrual cycle and 14 females in the second (luteal) phase of menstrual cycle upon hospitalization. The Hamilton scale was used to determine degree of depressive state upon hospitalization an after 28 days. At both time points, blood was sampled and level of testosterone and estrogen for male and estrogen, progesterone and testosterone for female patients was analysed. Results of the study showed that antidepressant effect calculated as a difference in Hamilton scale was highest in male group of patients and significantly higher than in women in the second phase of the cycle (10.4 vs 8.1). This correlated with increase of testosterone in male patients during four weeks treatment (12.08 vs. 9.46), while there was no significant change in the level of testosterone in both female groups of patients. Furthermore, in female patients in the luteal phase of the cycle, with lowest response to antidepressants, both estrogen and progesterone were significantly reduced during four weeks of treatment. In conclusion, results of our pilot study suggest sex differences in response to antidepressant therapy and level of hormonal status should be evaluated for better personalized pharmacotherapy.",
publisher = "John Wiley & Sons, Inc",
journal = "FEBS Open Bio",
title = "Sex steroid hormones status influence on
antidepressant pharmacotherapy effect in
male and female patients",
volume = "12",
number = "S1",
pages = "325-325",
doi = "10.1002/2211-5463.13440"
}

Pejušković, B., Lero, M., Đekić, J., Nikolašević, G., Dobrosavljević, A., Petrović, J.,& Pešić, V.. (2022). Sex steroid hormones status influence on
antidepressant pharmacotherapy effect in
male and female patients. in FEBS Open Bio
John Wiley & Sons, Inc., 12(S1), 325-325.
https://doi.org/10.1002/2211-5463.13440

Pejušković B, Lero M, Đekić J, Nikolašević G, Dobrosavljević A, Petrović J, Pešić V. Sex steroid hormones status influence on
antidepressant pharmacotherapy effect in
male and female patients. in FEBS Open Bio. 2022;12(S1):325-325.
doi:10.1002/2211-5463.13440 .

Pejušković, Bojana, Lero, M., Đekić, J., Nikolašević, Gorana, Dobrosavljević, Ana, Petrović, Jelena, Pešić, Vesna, "Sex steroid hormones status influence on
antidepressant pharmacotherapy effect in
male and female patients" in FEBS Open Bio, 12, no. S1 (2022):325-325,
https://doi.org/10.1002/2211-5463.13440 . .

TY  - CONF
AU  - Milosavljević, Filip
AU  - Brusini, Irene
AU  - Atanasov, Andrea
AU  - Manojlović, Marina
AU  - Vučić, Marija
AU  - Oreščanin-Dušić, Zorana
AU  - Brkljačić, Jelena
AU  - Sitarica, Pavle
AU  - Miljević, Čedo
AU  - Nikolić-Kokić, Aleksandra
AU  - Blagojević, Duško
AU  - Wang, Chunliang
AU  - Damberg, Peter
AU  - Pešić, Vesna
AU  - Tyndale, Rachel
AU  - Ingelman-Sundberg, Magnus
AU  - Jukić, Marin
PY  - 2022
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4729
AB  - Background: Animal models are essential for understanding aetiology and pathophysiology of movement disorders. Previously, it had been found that mice transgenic for the human CYP2C19 gene, which is expressed in the liver and developing brain, exhibit altered neurodevelopment associated with impairments of their motor function and emotionality [1, 2]. The aim of this study was to characterize motoric phenotype of the CYP2C19 transgenic mouse and validate its potential usefulness as an animal model for ataxia.

Methods: Experiments were performed on CYP2C19 transgenic mice and control wild-type littermate mice. Body weight of mice was measured between the 21st and 42nd postnatal day. Mouse gait was analysed with footprint test [3] in young animals at four time points and once in adult mice. The maximal height of hindpaw elevation while walking was measured offline from the video footage of the footprint test. Motoric function was quantified by the rotarod and beam-walking tests. Structural differences in 20 brain regions of wild-type and transgenic mice were investigated with 9.4T gadolinium-enhanced postmortem neuroimaging. Antioxidative enzyme status was determined in the brain tissue in order to assess potential differences in the brain oxidative-antioxidative balance between wild-type and transgenic mice. When multiple brain regions or multiple antioxidant enzyme activities were analysed, p-values were FDR corrected for multiple comparisons.

Results: CYP2C19 transgenic (TG) animals exhibited approximately 5-10% reduced body weight (p=0.015) during 3rd and 4th postnatal week, while after postnatal day 31, the differences in the body weight were no longer statistically significant. The TG animals exhibited approximately two fold higher maximal hindpaw elevation in young (2.1-fold [CI95%: 2.0, 2.2], p<0.0001) and adult mice (1.9-fold [CI95%: 1.8, 2.1], p<0.0001), compared to wild-types. In the 5th postnatal week, all transgenic mice exhibited increase in elevation of both hindpaws, while after this point they gradually started exhibiting unilateral phenotype until almost all (49 of 51) animals became unilaterally affected in the adulthood. Footprint analysis and rotarod test did not detect significant differences (p>0.1) between TG and control mice in any of the analysed parameters, accounting for all examined time points. CYP2C19 transgenic mice exhibited 14% increase in beam crossing time (14%, [95%CI: 6.4, 22], p=0.0014) and 5.6-fold more paw-slips (p<0.0001, n=89) in the beam-walking test. CYP2C19 transgenic mice exhibited profound reduction in cerebellar volume (-11.8% [95%CI: -14.7, -9.0], q<0.0001, n=59) and moderate reduction in hippocampal volume (-4.2% [95%CI: -6.4%, -1.9%], q=0.015, n=59); compared to the corresponding volumes measured in WT mice. Superoxide dismutase activity was slightly increased (1.14-fold [CI95%: 1.06, 1.23], p=0.0010, q=0.023) in the cerebelli and moderately increased (1.3-fold, [CI95%: 1.18, 1.47], p<0.0001, q=0.0013) in the hippocampi of transgenic mice compared to wild-types, while glutathione reductase activity was significantly increased (1.2-fold [CI95%: 1.13, 1.35], p<0.0001, q=0.0021) in the hippocampi of TG mice.

Conclusions: Humanized CYP2C19 transgenic mice exhibit altered motoric function, functional motoric impairments and reduced cerebellar volume. CYP2C19 transgenic mice can be a useful tool for the studies focused on understanding the physiology of cerebellar development, as well as aetiology and pathophysiology of cerebellum-related disorders.
PB  - Elsevier
C3  - Neuroscience Applied
T1  - Humanized CYP2C19 transgenic mouse as an animal model of cerebellar ataxia
VL  - 1
IS  - Supplement 2
SP  - 64
EP  - 64
DO  - 10.1016/j.nsa.2022.100236
ER  - 

@conference{
author = "Milosavljević, Filip and Brusini, Irene and Atanasov, Andrea and Manojlović, Marina and Vučić, Marija and Oreščanin-Dušić, Zorana and Brkljačić, Jelena and Sitarica, Pavle and Miljević, Čedo and Nikolić-Kokić, Aleksandra and Blagojević, Duško and Wang, Chunliang and Damberg, Peter and Pešić, Vesna and Tyndale, Rachel and Ingelman-Sundberg, Magnus and Jukić, Marin",
year = "2022",
abstract = "Background: Animal models are essential for understanding aetiology and pathophysiology of movement disorders. Previously, it had been found that mice transgenic for the human CYP2C19 gene, which is expressed in the liver and developing brain, exhibit altered neurodevelopment associated with impairments of their motor function and emotionality [1, 2]. The aim of this study was to characterize motoric phenotype of the CYP2C19 transgenic mouse and validate its potential usefulness as an animal model for ataxia.

Methods: Experiments were performed on CYP2C19 transgenic mice and control wild-type littermate mice. Body weight of mice was measured between the 21st and 42nd postnatal day. Mouse gait was analysed with footprint test [3] in young animals at four time points and once in adult mice. The maximal height of hindpaw elevation while walking was measured offline from the video footage of the footprint test. Motoric function was quantified by the rotarod and beam-walking tests. Structural differences in 20 brain regions of wild-type and transgenic mice were investigated with 9.4T gadolinium-enhanced postmortem neuroimaging. Antioxidative enzyme status was determined in the brain tissue in order to assess potential differences in the brain oxidative-antioxidative balance between wild-type and transgenic mice. When multiple brain regions or multiple antioxidant enzyme activities were analysed, p-values were FDR corrected for multiple comparisons.

Results: CYP2C19 transgenic (TG) animals exhibited approximately 5-10% reduced body weight (p=0.015) during 3rd and 4th postnatal week, while after postnatal day 31, the differences in the body weight were no longer statistically significant. The TG animals exhibited approximately two fold higher maximal hindpaw elevation in young (2.1-fold [CI95%: 2.0, 2.2], p<0.0001) and adult mice (1.9-fold [CI95%: 1.8, 2.1], p<0.0001), compared to wild-types. In the 5th postnatal week, all transgenic mice exhibited increase in elevation of both hindpaws, while after this point they gradually started exhibiting unilateral phenotype until almost all (49 of 51) animals became unilaterally affected in the adulthood. Footprint analysis and rotarod test did not detect significant differences (p>0.1) between TG and control mice in any of the analysed parameters, accounting for all examined time points. CYP2C19 transgenic mice exhibited 14% increase in beam crossing time (14%, [95%CI: 6.4, 22], p=0.0014) and 5.6-fold more paw-slips (p<0.0001, n=89) in the beam-walking test. CYP2C19 transgenic mice exhibited profound reduction in cerebellar volume (-11.8% [95%CI: -14.7, -9.0], q<0.0001, n=59) and moderate reduction in hippocampal volume (-4.2% [95%CI: -6.4%, -1.9%], q=0.015, n=59); compared to the corresponding volumes measured in WT mice. Superoxide dismutase activity was slightly increased (1.14-fold [CI95%: 1.06, 1.23], p=0.0010, q=0.023) in the cerebelli and moderately increased (1.3-fold, [CI95%: 1.18, 1.47], p<0.0001, q=0.0013) in the hippocampi of transgenic mice compared to wild-types, while glutathione reductase activity was significantly increased (1.2-fold [CI95%: 1.13, 1.35], p<0.0001, q=0.0021) in the hippocampi of TG mice.

Conclusions: Humanized CYP2C19 transgenic mice exhibit altered motoric function, functional motoric impairments and reduced cerebellar volume. CYP2C19 transgenic mice can be a useful tool for the studies focused on understanding the physiology of cerebellar development, as well as aetiology and pathophysiology of cerebellum-related disorders.",
publisher = "Elsevier",
journal = "Neuroscience Applied",
title = "Humanized CYP2C19 transgenic mouse as an animal model of cerebellar ataxia",
volume = "1",
number = "Supplement 2",
pages = "64-64",
doi = "10.1016/j.nsa.2022.100236"
}

Milosavljević, F., Brusini, I., Atanasov, A., Manojlović, M., Vučić, M., Oreščanin-Dušić, Z., Brkljačić, J., Sitarica, P., Miljević, Č., Nikolić-Kokić, A., Blagojević, D., Wang, C., Damberg, P., Pešić, V., Tyndale, R., Ingelman-Sundberg, M.,& Jukić, M.. (2022). Humanized CYP2C19 transgenic mouse as an animal model of cerebellar ataxia. in Neuroscience Applied
Elsevier., 1(Supplement 2), 64-64.
https://doi.org/10.1016/j.nsa.2022.100236

Milosavljević F, Brusini I, Atanasov A, Manojlović M, Vučić M, Oreščanin-Dušić Z, Brkljačić J, Sitarica P, Miljević Č, Nikolić-Kokić A, Blagojević D, Wang C, Damberg P, Pešić V, Tyndale R, Ingelman-Sundberg M, Jukić M. Humanized CYP2C19 transgenic mouse as an animal model of cerebellar ataxia. in Neuroscience Applied. 2022;1(Supplement 2):64-64.
doi:10.1016/j.nsa.2022.100236 .

Milosavljević, Filip, Brusini, Irene, Atanasov, Andrea, Manojlović, Marina, Vučić, Marija, Oreščanin-Dušić, Zorana, Brkljačić, Jelena, Sitarica, Pavle, Miljević, Čedo, Nikolić-Kokić, Aleksandra, Blagojević, Duško, Wang, Chunliang, Damberg, Peter, Pešić, Vesna, Tyndale, Rachel, Ingelman-Sundberg, Magnus, Jukić, Marin, "Humanized CYP2C19 transgenic mouse as an animal model of cerebellar ataxia" in Neuroscience Applied, 1, no. Supplement 2 (2022):64-64,
https://doi.org/10.1016/j.nsa.2022.100236 . .

TY  - JOUR
AU  - Dangoor, Itzhak
AU  - Stanić, Dušanka
AU  - Reshef, Leah
AU  - Pešić, Vesna
AU  - Gophna, Uri
PY  - 2021
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3965
AB  - Humans are colonized by bacteria, fungi, archaea, and viruses, which are collectively referred to as the microbiome. Most of the microbiome resides in the gut and may easily be investigated via stool sampling and subsequent metagenomic DNA sequencing. Prolonged exposure to psychiatric pharmacological agents is often associated with marked gastrointestinal phenomena, including changes in food intake, bowel motility, gastric emptying, and transit time [1–3]. Unlike the relatively objective measurement of the microbiota composition, accurate assessment of patients’ therapy adherence and treatment outcomes represent a challenge in psychiatric medical care [4]. This is partly because, for most psychopharmacological agents, compliance and response to treatments are subjectively assessed based on self-reporting and physicians’ evaluations [5,6]. An interesting alternative is having changes in the psychiatric patients’ gut microbiota composition serve as a measurable proxy for monitoring patients’ compliance and the therapeutic effects of some drugs. It is yet unclear how behavioral changes and drug intake affect the microbiota; however, mounting evidence suggests that physical and mental disturbances may lead to changes in gastrointestinal (GI) motility [7,8] in both animals and humans [9–11]. Indeed, in humans, anger, fear, pain, and anxiety, as well as intensive exercise, results in changes in GI activity [8]. In rats, chronic stress results in initial delayed gastric emptying followed by acceleration later on [12]. Medication intake [13,14] and changes in stool consistency, gastric transit, and emptying time [15,16] also have a great impact on microbial composition.
PB  - MDPI
T2  - Microorganisms
T1  - Specific changes in the mammalian gut microbiome as a biomarker for oxytocin-induced behavioral changes
VL  - 9
IS  - 9
DO  - 10.3390/microorganisms9091938
ER  - 

@article{
author = "Dangoor, Itzhak and Stanić, Dušanka and Reshef, Leah and Pešić, Vesna and Gophna, Uri",
year = "2021",
abstract = "Humans are colonized by bacteria, fungi, archaea, and viruses, which are collectively referred to as the microbiome. Most of the microbiome resides in the gut and may easily be investigated via stool sampling and subsequent metagenomic DNA sequencing. Prolonged exposure to psychiatric pharmacological agents is often associated with marked gastrointestinal phenomena, including changes in food intake, bowel motility, gastric emptying, and transit time [1–3]. Unlike the relatively objective measurement of the microbiota composition, accurate assessment of patients’ therapy adherence and treatment outcomes represent a challenge in psychiatric medical care [4]. This is partly because, for most psychopharmacological agents, compliance and response to treatments are subjectively assessed based on self-reporting and physicians’ evaluations [5,6]. An interesting alternative is having changes in the psychiatric patients’ gut microbiota composition serve as a measurable proxy for monitoring patients’ compliance and the therapeutic effects of some drugs. It is yet unclear how behavioral changes and drug intake affect the microbiota; however, mounting evidence suggests that physical and mental disturbances may lead to changes in gastrointestinal (GI) motility [7,8] in both animals and humans [9–11]. Indeed, in humans, anger, fear, pain, and anxiety, as well as intensive exercise, results in changes in GI activity [8]. In rats, chronic stress results in initial delayed gastric emptying followed by acceleration later on [12]. Medication intake [13,14] and changes in stool consistency, gastric transit, and emptying time [15,16] also have a great impact on microbial composition.",
publisher = "MDPI",
journal = "Microorganisms",
title = "Specific changes in the mammalian gut microbiome as a biomarker for oxytocin-induced behavioral changes",
volume = "9",
number = "9",
doi = "10.3390/microorganisms9091938"
}

Dangoor, I., Stanić, D., Reshef, L., Pešić, V.,& Gophna, U.. (2021). Specific changes in the mammalian gut microbiome as a biomarker for oxytocin-induced behavioral changes. in Microorganisms
MDPI., 9(9).
https://doi.org/10.3390/microorganisms9091938

Dangoor I, Stanić D, Reshef L, Pešić V, Gophna U. Specific changes in the mammalian gut microbiome as a biomarker for oxytocin-induced behavioral changes. in Microorganisms. 2021;9(9).
doi:10.3390/microorganisms9091938 .

Dangoor, Itzhak, Stanić, Dušanka, Reshef, Leah, Pešić, Vesna, Gophna, Uri, "Specific changes in the mammalian gut microbiome as a biomarker for oxytocin-induced behavioral changes" in Microorganisms, 9, no. 9 (2021),
https://doi.org/10.3390/microorganisms9091938 . .

TY  - JOUR
AU  - Stanić, Dušanka
AU  - Oved, Keren
AU  - Israel-Elgali, Ifat
AU  - Jukić, Marin
AU  - Batinić, Bojan
AU  - Puškaš, Nela
AU  - Shomron, Noam
AU  - Gurwitz, David
AU  - Pešić, Vesna
PY  - 2021
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3883
AB  - Intranasal treatment with oxytocin showed beneficial effects in post-traumatic stress disorder and autism spectrum disorders; however, it was not investigated as much in depression. Keeping in mind the favorable effects of oxytocin on animal models of anxiety and depression, we postulated that synergy between prescribed first choice drugs, selective serotonin reuptake inhibitors (SSRIs) and oxytocin could improve the treatment outcome compared with SSRI monotherapy. Our previous in vitro genome-wide transcriptomic study on human lymphoblastoid cell lines exposed to paroxetine resulted in increase of integrin β3 (ITGB3) gene expression, and further, ITGB3/CHL1 expression ratio was hypothesized to influence the sensitivity to SSRIs. The aim of this report was to explore molecular mechanisms behind the antidepressant-like oxytocin effect, alone and in synergy with citalopram, on behavioral and molecular level in corticosterone treated rats, a paradigm used to model anxiety and depression in animals. Oxytocin treatment (1) ameliorated corticosterone-induced reduction of neurogenesis and number of parvalbumin-positive interneurons in the hippocampal CA1 region, (2) enhanced anxiolytic- and antidepressant-like effects of citalopram in the open field test, and (3) the SSRI/oxytocin synergy persisted in reversing the reduction of the Itgb3 gene expression and increased Itgb3/Chl1 ratio in the prefrontal cortices. These results support the existence of synergy between citalopram and oxytocin in reversing the molecular and behavioral changes induced by corticosterone treatment and point to possible molecular mechanisms behind antidepressant-like effect of oxytocin.
PB  - Elsevier Ltd
T2  - Psychoneuroendocrinology
T1  - Synergy of oxytocin and citalopram in modulating Itgb3/Chl1 interplay: Relevance to sensitivity to SSRI therapy
VL  - 129
DO  - 10.1016/j.psyneuen.2021.105234
ER  - 

@article{
author = "Stanić, Dušanka and Oved, Keren and Israel-Elgali, Ifat and Jukić, Marin and Batinić, Bojan and Puškaš, Nela and Shomron, Noam and Gurwitz, David and Pešić, Vesna",
year = "2021",
abstract = "Intranasal treatment with oxytocin showed beneficial effects in post-traumatic stress disorder and autism spectrum disorders; however, it was not investigated as much in depression. Keeping in mind the favorable effects of oxytocin on animal models of anxiety and depression, we postulated that synergy between prescribed first choice drugs, selective serotonin reuptake inhibitors (SSRIs) and oxytocin could improve the treatment outcome compared with SSRI monotherapy. Our previous in vitro genome-wide transcriptomic study on human lymphoblastoid cell lines exposed to paroxetine resulted in increase of integrin β3 (ITGB3) gene expression, and further, ITGB3/CHL1 expression ratio was hypothesized to influence the sensitivity to SSRIs. The aim of this report was to explore molecular mechanisms behind the antidepressant-like oxytocin effect, alone and in synergy with citalopram, on behavioral and molecular level in corticosterone treated rats, a paradigm used to model anxiety and depression in animals. Oxytocin treatment (1) ameliorated corticosterone-induced reduction of neurogenesis and number of parvalbumin-positive interneurons in the hippocampal CA1 region, (2) enhanced anxiolytic- and antidepressant-like effects of citalopram in the open field test, and (3) the SSRI/oxytocin synergy persisted in reversing the reduction of the Itgb3 gene expression and increased Itgb3/Chl1 ratio in the prefrontal cortices. These results support the existence of synergy between citalopram and oxytocin in reversing the molecular and behavioral changes induced by corticosterone treatment and point to possible molecular mechanisms behind antidepressant-like effect of oxytocin.",
publisher = "Elsevier Ltd",
journal = "Psychoneuroendocrinology",
title = "Synergy of oxytocin and citalopram in modulating Itgb3/Chl1 interplay: Relevance to sensitivity to SSRI therapy",
volume = "129",
doi = "10.1016/j.psyneuen.2021.105234"
}

Stanić, D., Oved, K., Israel-Elgali, I., Jukić, M., Batinić, B., Puškaš, N., Shomron, N., Gurwitz, D.,& Pešić, V.. (2021). Synergy of oxytocin and citalopram in modulating Itgb3/Chl1 interplay: Relevance to sensitivity to SSRI therapy. in Psychoneuroendocrinology
Elsevier Ltd., 129.
https://doi.org/10.1016/j.psyneuen.2021.105234

Stanić D, Oved K, Israel-Elgali I, Jukić M, Batinić B, Puškaš N, Shomron N, Gurwitz D, Pešić V. Synergy of oxytocin and citalopram in modulating Itgb3/Chl1 interplay: Relevance to sensitivity to SSRI therapy. in Psychoneuroendocrinology. 2021;129.
doi:10.1016/j.psyneuen.2021.105234 .

Stanić, Dušanka, Oved, Keren, Israel-Elgali, Ifat, Jukić, Marin, Batinić, Bojan, Puškaš, Nela, Shomron, Noam, Gurwitz, David, Pešić, Vesna, "Synergy of oxytocin and citalopram in modulating Itgb3/Chl1 interplay: Relevance to sensitivity to SSRI therapy" in Psychoneuroendocrinology, 129 (2021),
https://doi.org/10.1016/j.psyneuen.2021.105234 . .

TY  - JOUR
AU  - Petrović, Jelena
AU  - Pešić, Vesna
AU  - Lauschke, Volker M.
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3501
AB  - CYP2C19 and CYP2D6 are important drug-metabolizing enzymes that are involved in the metabolism of around 30% of allmedications. Importantly, the corresponding genes are highly polymorphic and these genetic differences contribute tointerindividual and interethnic differences in drug pharmacokinetics, response, and toxicity. In this study we systematicallyanalyzed the frequency distribution of clinically relevantCYP2C19andCYP2D6alleles across Europe based on data from82,791 healthy individuals extracted from 79 original publications and, for thefirst time, provide allele confidence intervalsfor the general population. We found that frequencies ofCYP2D6gene duplications showed a clear South-East to North-West gradient ranging from <1% in Sweden and Denmark to 6% in Greece and Turkey. In contrast, an inverse distributionwas observed for the loss-of-function allelesCYP2D6*4andCYP2D6*5. Similarly, frequencies of the inactiveCYP2C19*2allele were graded from North-West to South-East Europe. In important contrast to previous work we found that theincreased activity alleleCYP2C19*17was most prevalent in Central Europe (25–33%) with lower prevalence inMediterranean-South Europeans (11–24%). In summary, we provide a detailed European map of commonCYP2C19andCYP2D6variants andfind that frequencies of the most clinically relevant alleles are geographically graded reflective ofEurope’s migratory history. Thesefindings emphasize the importance of generating pharmacogenomic data sets with highspatial resolution to improve precision public health across Europe.
PB  - Springer Nature
T2  - European Journal of Human Genetics
T1  - Frequencies of clinically important CYP2C19 and CYP2D6 alleles are graded across Europe
VL  - 28
IS  - 1
SP  - 88
EP  - 94
DO  - 10.1038/s41431-019-0480-8
ER  - 

@article{
author = "Petrović, Jelena and Pešić, Vesna and Lauschke, Volker M.",
year = "2020",
abstract = "CYP2C19 and CYP2D6 are important drug-metabolizing enzymes that are involved in the metabolism of around 30% of allmedications. Importantly, the corresponding genes are highly polymorphic and these genetic differences contribute tointerindividual and interethnic differences in drug pharmacokinetics, response, and toxicity. In this study we systematicallyanalyzed the frequency distribution of clinically relevantCYP2C19andCYP2D6alleles across Europe based on data from82,791 healthy individuals extracted from 79 original publications and, for thefirst time, provide allele confidence intervalsfor the general population. We found that frequencies ofCYP2D6gene duplications showed a clear South-East to North-West gradient ranging from <1% in Sweden and Denmark to 6% in Greece and Turkey. In contrast, an inverse distributionwas observed for the loss-of-function allelesCYP2D6*4andCYP2D6*5. Similarly, frequencies of the inactiveCYP2C19*2allele were graded from North-West to South-East Europe. In important contrast to previous work we found that theincreased activity alleleCYP2C19*17was most prevalent in Central Europe (25–33%) with lower prevalence inMediterranean-South Europeans (11–24%). In summary, we provide a detailed European map of commonCYP2C19andCYP2D6variants andfind that frequencies of the most clinically relevant alleles are geographically graded reflective ofEurope’s migratory history. Thesefindings emphasize the importance of generating pharmacogenomic data sets with highspatial resolution to improve precision public health across Europe.",
publisher = "Springer Nature",
journal = "European Journal of Human Genetics",
title = "Frequencies of clinically important CYP2C19 and CYP2D6 alleles are graded across Europe",
volume = "28",
number = "1",
pages = "88-94",
doi = "10.1038/s41431-019-0480-8"
}

Petrović, J., Pešić, V.,& Lauschke, V. M.. (2020). Frequencies of clinically important CYP2C19 and CYP2D6 alleles are graded across Europe. in European Journal of Human Genetics
Springer Nature., 28(1), 88-94.
https://doi.org/10.1038/s41431-019-0480-8

Petrović J, Pešić V, Lauschke VM. Frequencies of clinically important CYP2C19 and CYP2D6 alleles are graded across Europe. in European Journal of Human Genetics. 2020;28(1):88-94.
doi:10.1038/s41431-019-0480-8 .

Petrović, Jelena, Pešić, Vesna, Lauschke, Volker M., "Frequencies of clinically important CYP2C19 and CYP2D6 alleles are graded across Europe" in European Journal of Human Genetics, 28, no. 1 (2020):88-94,
https://doi.org/10.1038/s41431-019-0480-8 . .

TY  - CONF
AU  - Milosavljević, Filip
AU  - Bukvić, Nikola
AU  - Pavlović, Zorana
AU  - Miljević, Čedo
AU  - Pešić, Vesna
AU  - Molden, Espen
AU  - Ingelman-Sundberg, Magnus
AU  - Leucht, Stefan
AU  - Jukić, Marin
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4761
PB  - Elsevier
C3  - European Neuropsychopharmacology
T1  - Impact of CYP2C19 and CYP2D6 polymorphism on antidepressants and antipsychotics exposure; a meta-analysis
VL  - 40
IS  - Supplement 1
SP  - S250
EP  - S251
DO  - 10.1016/j.euroneuro.2020.09.325
ER  - 

@conference{
author = "Milosavljević, Filip and Bukvić, Nikola and Pavlović, Zorana and Miljević, Čedo and Pešić, Vesna and Molden, Espen and Ingelman-Sundberg, Magnus and Leucht, Stefan and Jukić, Marin",
year = "2020",
publisher = "Elsevier",
journal = "European Neuropsychopharmacology",
title = "Impact of CYP2C19 and CYP2D6 polymorphism on antidepressants and antipsychotics exposure; a meta-analysis",
volume = "40",
number = "Supplement 1",
pages = "S250-S251",
doi = "10.1016/j.euroneuro.2020.09.325"
}

Milosavljević, F., Bukvić, N., Pavlović, Z., Miljević, Č., Pešić, V., Molden, E., Ingelman-Sundberg, M., Leucht, S.,& Jukić, M.. (2020). Impact of CYP2C19 and CYP2D6 polymorphism on antidepressants and antipsychotics exposure; a meta-analysis. in European Neuropsychopharmacology
Elsevier., 40(Supplement 1), S250-S251.
https://doi.org/10.1016/j.euroneuro.2020.09.325

Milosavljević F, Bukvić N, Pavlović Z, Miljević Č, Pešić V, Molden E, Ingelman-Sundberg M, Leucht S, Jukić M. Impact of CYP2C19 and CYP2D6 polymorphism on antidepressants and antipsychotics exposure; a meta-analysis. in European Neuropsychopharmacology. 2020;40(Supplement 1):S250-S251.
doi:10.1016/j.euroneuro.2020.09.325 .

Milosavljević, Filip, Bukvić, Nikola, Pavlović, Zorana, Miljević, Čedo, Pešić, Vesna, Molden, Espen, Ingelman-Sundberg, Magnus, Leucht, Stefan, Jukić, Marin, "Impact of CYP2C19 and CYP2D6 polymorphism on antidepressants and antipsychotics exposure; a meta-analysis" in European Neuropsychopharmacology, 40, no. Supplement 1 (2020):S250-S251,
https://doi.org/10.1016/j.euroneuro.2020.09.325 . .

TY  - CONF
AU  - Milosavljević, Filip
AU  - Vučić, Marija
AU  - Manojlović, Marina
AU  - Miloševski, Teodora
AU  - Batinić, Bojan
AU  - Novalen, Maria
AU  - Miksys, Sharon
AU  - Tyndale, Rachel
AU  - Ingelman-Sundberg, Magnus
AU  - Pešić, Vesna
AU  - Jukić, Marin
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4753
AB  - Introduction: CYP2C19 transgenic mouse (2C19TG) is generated by the insertion of 12 copies of the human CYP2C19 gene into mouse genome. This animal model is a tool to study the neurodevelopmental role of CYP2C19 in vivo, since this enzyme is expressed in the foetal brains of 2C19TG mice and humans. Previous studies [1,2] showed anxiety and depression-like behaviour in these mice, while the aim of this study was to characterize the motoric function of the 2C19TG mouse.
Methods: Whole brain dopamine concentration was measured in the brain homogenate of 23 adult mice by the HPLC-MS method. Motoric function in 50 mutant and 43 control mice of both genders was tested by the rotarod and beam walking tests. Beam walking test was repeated after treatment with dopaminergic receptor antagonists, Ecopipam (0.1 mg/kg) and Raclopride (0.25 mg/kg) as a follow-up. The sections of 10 6-month old and 8 15-months old mice were stained with anti-tyrosine hydroxylase antibody and the number of dopaminergic neurons was counted on histological slides under microscope. Next, after transcardial perfusion of 30 2C19TG and 30 control mice of both genders with contrast agent (4% Paraformaldehyde, 0.05M Gadoteridole, 0.01M Phosphate buffered saline, pH=7.4), cranium containing the whole brain was scanned overnight by the 9.4T MRI scanner. The volumes of 39 brain regions were quantified according to the mouse brain atlas [3]. Student's t-test and two-way ANOVA were used to evaluate statistical significance of between-group differences.
Results: Adult 2C19TG mice are hyperdopaminergic, as they exhibit 15% increased dopamine concentration (p<0.001). They also show hyperkinetic motoric phenotype with the ataxia-like walking pattern and pathological clasping reflex. In the beam walking test 2C19TG mice had 20% longer beam crossing time (p=0.007) and 60% more paw slips (p<0.001) then the controls, and this motoric impairment could not be improved with antidopaminergic drugs. Both younger and older 2C19TG mice exhibited only a marginal reduction in the number of dopaminergic neurons of both substantia nigra and ventral tegmental area in a subset of coronal sections. This was confirmed by the gadolinium-enhanced neuroimaging that showed no change in substantia nigra volume in 2C19TG mice. On the other hand, significant differences in volume were identified in 11 regions, including cerebellum (-8.3% p<0.001) and striatum (+3.0%, p<0.001), which are the regions connected with the motoric function. The volumetric changes were detected in the hippocampus (-1.3%, p=0.027), amygdala (+2.8%, p<0.001), septum (+3.3%, p=0.014) and nucleus accumbens (+3.5, p=0.004) of 2C19TG mice. These brain regions are involved in emotional and motivational functions.
Conclusion: Ataxia-like motoric phenotype in 2C19TG transgenic mice is probably caused by changes in cerebellum, while hyperdopaminergism is most likely the compensatory adaptation, whereas the changes in the hippocampus, amygdala, septum, and nucleus accumbens may be connected with the mutants’ depression-like phenotype and susceptibility to stress. Therefore, CYP2C19 transgenic mouse in potentially useful model of hyperkinetic disorders, and our findings hint at the possible impact of CYP2C19 enzyme on the development of the several brain regions involved in motor and emotional functioning.
PB  - Elsevier
C3  - European Neuropsychopharmacology
T1  - Reduced cerebellum volume and ataxia-like motoric phenotype in transgenic mouse, carrier of human CYP2C19 gene
VL  - 40
IS  - 1
SP  - S207
EP  - S208
DO  - 10.1016/j.euroneuro.2020.09.271
ER  - 

@conference{
author = "Milosavljević, Filip and Vučić, Marija and Manojlović, Marina and Miloševski, Teodora and Batinić, Bojan and Novalen, Maria and Miksys, Sharon and Tyndale, Rachel and Ingelman-Sundberg, Magnus and Pešić, Vesna and Jukić, Marin",
year = "2020",
abstract = "Introduction: CYP2C19 transgenic mouse (2C19TG) is generated by the insertion of 12 copies of the human CYP2C19 gene into mouse genome. This animal model is a tool to study the neurodevelopmental role of CYP2C19 in vivo, since this enzyme is expressed in the foetal brains of 2C19TG mice and humans. Previous studies [1,2] showed anxiety and depression-like behaviour in these mice, while the aim of this study was to characterize the motoric function of the 2C19TG mouse.
Methods: Whole brain dopamine concentration was measured in the brain homogenate of 23 adult mice by the HPLC-MS method. Motoric function in 50 mutant and 43 control mice of both genders was tested by the rotarod and beam walking tests. Beam walking test was repeated after treatment with dopaminergic receptor antagonists, Ecopipam (0.1 mg/kg) and Raclopride (0.25 mg/kg) as a follow-up. The sections of 10 6-month old and 8 15-months old mice were stained with anti-tyrosine hydroxylase antibody and the number of dopaminergic neurons was counted on histological slides under microscope. Next, after transcardial perfusion of 30 2C19TG and 30 control mice of both genders with contrast agent (4% Paraformaldehyde, 0.05M Gadoteridole, 0.01M Phosphate buffered saline, pH=7.4), cranium containing the whole brain was scanned overnight by the 9.4T MRI scanner. The volumes of 39 brain regions were quantified according to the mouse brain atlas [3]. Student's t-test and two-way ANOVA were used to evaluate statistical significance of between-group differences.
Results: Adult 2C19TG mice are hyperdopaminergic, as they exhibit 15% increased dopamine concentration (p<0.001). They also show hyperkinetic motoric phenotype with the ataxia-like walking pattern and pathological clasping reflex. In the beam walking test 2C19TG mice had 20% longer beam crossing time (p=0.007) and 60% more paw slips (p<0.001) then the controls, and this motoric impairment could not be improved with antidopaminergic drugs. Both younger and older 2C19TG mice exhibited only a marginal reduction in the number of dopaminergic neurons of both substantia nigra and ventral tegmental area in a subset of coronal sections. This was confirmed by the gadolinium-enhanced neuroimaging that showed no change in substantia nigra volume in 2C19TG mice. On the other hand, significant differences in volume were identified in 11 regions, including cerebellum (-8.3% p<0.001) and striatum (+3.0%, p<0.001), which are the regions connected with the motoric function. The volumetric changes were detected in the hippocampus (-1.3%, p=0.027), amygdala (+2.8%, p<0.001), septum (+3.3%, p=0.014) and nucleus accumbens (+3.5, p=0.004) of 2C19TG mice. These brain regions are involved in emotional and motivational functions.
Conclusion: Ataxia-like motoric phenotype in 2C19TG transgenic mice is probably caused by changes in cerebellum, while hyperdopaminergism is most likely the compensatory adaptation, whereas the changes in the hippocampus, amygdala, septum, and nucleus accumbens may be connected with the mutants’ depression-like phenotype and susceptibility to stress. Therefore, CYP2C19 transgenic mouse in potentially useful model of hyperkinetic disorders, and our findings hint at the possible impact of CYP2C19 enzyme on the development of the several brain regions involved in motor and emotional functioning.",
publisher = "Elsevier",
journal = "European Neuropsychopharmacology",
title = "Reduced cerebellum volume and ataxia-like motoric phenotype in transgenic mouse, carrier of human CYP2C19 gene",
volume = "40",
number = "1",
pages = "S207-S208",
doi = "10.1016/j.euroneuro.2020.09.271"
}

Milosavljević, F., Vučić, M., Manojlović, M., Miloševski, T., Batinić, B., Novalen, M., Miksys, S., Tyndale, R., Ingelman-Sundberg, M., Pešić, V.,& Jukić, M.. (2020). Reduced cerebellum volume and ataxia-like motoric phenotype in transgenic mouse, carrier of human CYP2C19 gene. in European Neuropsychopharmacology
Elsevier., 40(1), S207-S208.
https://doi.org/10.1016/j.euroneuro.2020.09.271

Milosavljević F, Vučić M, Manojlović M, Miloševski T, Batinić B, Novalen M, Miksys S, Tyndale R, Ingelman-Sundberg M, Pešić V, Jukić M. Reduced cerebellum volume and ataxia-like motoric phenotype in transgenic mouse, carrier of human CYP2C19 gene. in European Neuropsychopharmacology. 2020;40(1):S207-S208.
doi:10.1016/j.euroneuro.2020.09.271 .

Milosavljević, Filip, Vučić, Marija, Manojlović, Marina, Miloševski, Teodora, Batinić, Bojan, Novalen, Maria, Miksys, Sharon, Tyndale, Rachel, Ingelman-Sundberg, Magnus, Pešić, Vesna, Jukić, Marin, "Reduced cerebellum volume and ataxia-like motoric phenotype in transgenic mouse, carrier of human CYP2C19 gene" in European Neuropsychopharmacology, 40, no. 1 (2020):S207-S208,
https://doi.org/10.1016/j.euroneuro.2020.09.271 . .

TY  - CONF
AU  - Pešić, Vesna
AU  - Dobrosavljević, Ana
AU  - Stanić, Dušanka
AU  - Batinić, Bojan
AU  - Plećaš, Bosiljka
PY  - 2019
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3299
PB  - Elsevier Science BV, Amsterdam
C3  - European Neuropsychopharmacology
T1  - Ketamine in a model of depression resistant to tricyclic antidepressants
VL  - 29
IS  - Supplement 1
SP  - S271
EP  - S271
DO  - 10.1016/j.euroneuro.2018.11.430
ER  - 

@conference{
author = "Pešić, Vesna and Dobrosavljević, Ana and Stanić, Dušanka and Batinić, Bojan and Plećaš, Bosiljka",
year = "2019",
publisher = "Elsevier Science BV, Amsterdam",
journal = "European Neuropsychopharmacology",
title = "Ketamine in a model of depression resistant to tricyclic antidepressants",
volume = "29",
number = "Supplement 1",
pages = "S271-S271",
doi = "10.1016/j.euroneuro.2018.11.430"
}

Pešić, V., Dobrosavljević, A., Stanić, D., Batinić, B.,& Plećaš, B.. (2019). Ketamine in a model of depression resistant to tricyclic antidepressants. in European Neuropsychopharmacology
Elsevier Science BV, Amsterdam., 29(Supplement 1), S271-S271.
https://doi.org/10.1016/j.euroneuro.2018.11.430

Pešić V, Dobrosavljević A, Stanić D, Batinić B, Plećaš B. Ketamine in a model of depression resistant to tricyclic antidepressants. in European Neuropsychopharmacology. 2019;29(Supplement 1):S271-S271.
doi:10.1016/j.euroneuro.2018.11.430 .

Pešić, Vesna, Dobrosavljević, Ana, Stanić, Dušanka, Batinić, Bojan, Plećaš, Bosiljka, "Ketamine in a model of depression resistant to tricyclic antidepressants" in European Neuropsychopharmacology, 29, no. Supplement 1 (2019):S271-S271,
https://doi.org/10.1016/j.euroneuro.2018.11.430 . .

TY  - CONF
AU  - Milosavljević, Filip
AU  - Bukvić, Nikola
AU  - Pešić, Vesna
AU  - Pavlović, Zorana
AU  - Miljević, Čedo
AU  - Molden, Espen
AU  - Ingelman-Sundberg, Magnus
AU  - Jukić, Marin
PY  - 2019
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4752
PB  - Springer Nature
C3  - Neuropsychopharmacology
T1  - Quantification of Antidepressant and Antipsychotic Exposure Increase Caused by CYP2C19 and CYP2D6 Intermediate and Poor Metabolizer Status
IS  - 44
SP  - 139
DO  - 10.1038/s41386-019-0545-y
ER  - 

@conference{
author = "Milosavljević, Filip and Bukvić, Nikola and Pešić, Vesna and Pavlović, Zorana and Miljević, Čedo and Molden, Espen and Ingelman-Sundberg, Magnus and Jukić, Marin",
year = "2019",
publisher = "Springer Nature",
journal = "Neuropsychopharmacology",
title = "Quantification of Antidepressant and Antipsychotic Exposure Increase Caused by CYP2C19 and CYP2D6 Intermediate and Poor Metabolizer Status",
number = "44",
pages = "139",
doi = "10.1038/s41386-019-0545-y"
}

Milosavljević, F., Bukvić, N., Pešić, V., Pavlović, Z., Miljević, Č., Molden, E., Ingelman-Sundberg, M.,& Jukić, M.. (2019). Quantification of Antidepressant and Antipsychotic Exposure Increase Caused by CYP2C19 and CYP2D6 Intermediate and Poor Metabolizer Status. in Neuropsychopharmacology
Springer Nature.(44), 139.
https://doi.org/10.1038/s41386-019-0545-y

Milosavljević F, Bukvić N, Pešić V, Pavlović Z, Miljević Č, Molden E, Ingelman-Sundberg M, Jukić M. Quantification of Antidepressant and Antipsychotic Exposure Increase Caused by CYP2C19 and CYP2D6 Intermediate and Poor Metabolizer Status. in Neuropsychopharmacology. 2019;(44):139.
doi:10.1038/s41386-019-0545-y .

Milosavljević, Filip, Bukvić, Nikola, Pešić, Vesna, Pavlović, Zorana, Miljević, Čedo, Molden, Espen, Ingelman-Sundberg, Magnus, Jukić, Marin, "Quantification of Antidepressant and Antipsychotic Exposure Increase Caused by CYP2C19 and CYP2D6 Intermediate and Poor Metabolizer Status" in Neuropsychopharmacology, no. 44 (2019):139,
https://doi.org/10.1038/s41386-019-0545-y . .

TY  - CONF
AU  - Milosavljević, Filip
AU  - Bukvić, Nikola
AU  - Pešić, Vesna
AU  - Molden, Espen
AU  - Ingelman-Sundberg, Magnus
AU  - Jukić, Marin
PY  - 2019
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/4754
AB  - Introduction: Most of the antipsychotics and antidepressants are metabolized by CYP2C19 and CYP2D6 enzymes. Both CYP2D6 and CYP2C19 genes are polymorphic and metabolic capacity of the enzymes is genotype-determined. Homozygous null allele carriers do not possess active enzyme, and they are referred to as CYP2C19 or CYP2D6 poor metabolizers (PM). Certain genotypes do not abolish the enzyme completely, but they do cause drastic reduction of metabolic capacity and carriers of such genotypes are referred to as intermediate metabolizers (IM). It is known that CYP2C19 and CYP2D6 PM and IM status cause increase in exposure of certain antidepressants and antipsychotics; however, due to small sample size of the previously published studies, the magnitude of this effect still cannot be estimated with sufficient precision. Therefore, the aim of this meta-analysis was to pool all these studies and estimate the magnitude of drug exposure increase caused by CYP2C19 and CYP2D6 PM and IM status, compared with normal metabolizers (NM) to the best possible degree.
Methods: The inclusion of the drugs used for the literature survey for meta-analysis was based on the list of new generation antidepressants [1] and antipsychotics [2]. These drugs were screened for inclusion by the PubMed search *DrugName AND (CYP2C19 OR CYP2D6). The studies were included in the meta-analysis if (1) the patients were genotyped for CYP2C19 or CYP2D6; (2) adequate sorting of patients into NM, IM, and PM was possible; (3) the study included at least three patients per subgroup; and (4) drug exposure was measured in representative way by: (a) dose normalized area under plasma level (time) curve, (b) dose normalized steady state plasma levels, or (c) apparent total clearance of the drug from plasma after oral administration (CL/F, reciprocal value represented the drug exposure). Meta-analysis for a specific drug was performed if three or more studies met the inclusion criteria. Drug exposure head-to-head comparisons were made between PM or IM subjects and the NM subject group, which served as a reference. Heterogeneity across the studies was assessed using Cochran's Q test at a given significance level and the percentage of total variability across the studies attributable to heterogeneity was quantified using I2 value. Magnitude of increase is presented as: Odds ratio (95% Confidence interval)
Results: Based on the outcome of the literature survey, it was possible to perform meta-analysis for escitalopram, venlafaxine, risperidone, and aripiprazole. Escitalopram exposure was 1.37-fold (1.30-1.44) increased in CYP2C19 IM and 2.44-fold (2.27-2.61) increased in CYP2C19 PM. Venlafaxine exposure was not significantly changed in CYP2D6 PM, 1.10 (0.99-1.22). Risperidone and aripiprazole exposure increased was similar for CYP2D6 IM and PM. Risperidone exposure was 1.42 (1.36-1.51) increased in CYP2D6 IM and PM admixed. Aripiprazole exposure was 1.52 (1.45-1.58) increased in CYP2D6 IM and PM admixed.
Conclusions: According to the results, reducing escitalopram dose by 60% in CYP2C19 PM and by 30% in CYP2C19 IM are appropriate dosing decision. Next, reducing risperidone and aripiprazole dose by 30% in CYP2D6 PM is appropriate dosing decision. Finallytract, CYP2D6 metabolizer status is not clinically relevant in venlafaxine dosing.
PB  - Elsevier
C3  - European Neuropsychopharmacology
T1  - Quantification of antidepressant and antipsychotic exposure increase caused by CYP2C19 and CYP2D6 intermediate and poor metabolizer status by meta-analysis
VL  - 29
IS  - 6
SP  - S533
EP  - S534
DO  - 10.1016/j.euroneuro.2019.09.824
ER  - 

@conference{
author = "Milosavljević, Filip and Bukvić, Nikola and Pešić, Vesna and Molden, Espen and Ingelman-Sundberg, Magnus and Jukić, Marin",
year = "2019",
abstract = "Introduction: Most of the antipsychotics and antidepressants are metabolized by CYP2C19 and CYP2D6 enzymes. Both CYP2D6 and CYP2C19 genes are polymorphic and metabolic capacity of the enzymes is genotype-determined. Homozygous null allele carriers do not possess active enzyme, and they are referred to as CYP2C19 or CYP2D6 poor metabolizers (PM). Certain genotypes do not abolish the enzyme completely, but they do cause drastic reduction of metabolic capacity and carriers of such genotypes are referred to as intermediate metabolizers (IM). It is known that CYP2C19 and CYP2D6 PM and IM status cause increase in exposure of certain antidepressants and antipsychotics; however, due to small sample size of the previously published studies, the magnitude of this effect still cannot be estimated with sufficient precision. Therefore, the aim of this meta-analysis was to pool all these studies and estimate the magnitude of drug exposure increase caused by CYP2C19 and CYP2D6 PM and IM status, compared with normal metabolizers (NM) to the best possible degree.
Methods: The inclusion of the drugs used for the literature survey for meta-analysis was based on the list of new generation antidepressants [1] and antipsychotics [2]. These drugs were screened for inclusion by the PubMed search *DrugName AND (CYP2C19 OR CYP2D6). The studies were included in the meta-analysis if (1) the patients were genotyped for CYP2C19 or CYP2D6; (2) adequate sorting of patients into NM, IM, and PM was possible; (3) the study included at least three patients per subgroup; and (4) drug exposure was measured in representative way by: (a) dose normalized area under plasma level (time) curve, (b) dose normalized steady state plasma levels, or (c) apparent total clearance of the drug from plasma after oral administration (CL/F, reciprocal value represented the drug exposure). Meta-analysis for a specific drug was performed if three or more studies met the inclusion criteria. Drug exposure head-to-head comparisons were made between PM or IM subjects and the NM subject group, which served as a reference. Heterogeneity across the studies was assessed using Cochran's Q test at a given significance level and the percentage of total variability across the studies attributable to heterogeneity was quantified using I2 value. Magnitude of increase is presented as: Odds ratio (95% Confidence interval)
Results: Based on the outcome of the literature survey, it was possible to perform meta-analysis for escitalopram, venlafaxine, risperidone, and aripiprazole. Escitalopram exposure was 1.37-fold (1.30-1.44) increased in CYP2C19 IM and 2.44-fold (2.27-2.61) increased in CYP2C19 PM. Venlafaxine exposure was not significantly changed in CYP2D6 PM, 1.10 (0.99-1.22). Risperidone and aripiprazole exposure increased was similar for CYP2D6 IM and PM. Risperidone exposure was 1.42 (1.36-1.51) increased in CYP2D6 IM and PM admixed. Aripiprazole exposure was 1.52 (1.45-1.58) increased in CYP2D6 IM and PM admixed.
Conclusions: According to the results, reducing escitalopram dose by 60% in CYP2C19 PM and by 30% in CYP2C19 IM are appropriate dosing decision. Next, reducing risperidone and aripiprazole dose by 30% in CYP2D6 PM is appropriate dosing decision. Finallytract, CYP2D6 metabolizer status is not clinically relevant in venlafaxine dosing.",
publisher = "Elsevier",
journal = "European Neuropsychopharmacology",
title = "Quantification of antidepressant and antipsychotic exposure increase caused by CYP2C19 and CYP2D6 intermediate and poor metabolizer status by meta-analysis",
volume = "29",
number = "6",
pages = "S533-S534",
doi = "10.1016/j.euroneuro.2019.09.824"
}

Milosavljević, F., Bukvić, N., Pešić, V., Molden, E., Ingelman-Sundberg, M.,& Jukić, M.. (2019). Quantification of antidepressant and antipsychotic exposure increase caused by CYP2C19 and CYP2D6 intermediate and poor metabolizer status by meta-analysis. in European Neuropsychopharmacology
Elsevier., 29(6), S533-S534.
https://doi.org/10.1016/j.euroneuro.2019.09.824

Milosavljević F, Bukvić N, Pešić V, Molden E, Ingelman-Sundberg M, Jukić M. Quantification of antidepressant and antipsychotic exposure increase caused by CYP2C19 and CYP2D6 intermediate and poor metabolizer status by meta-analysis. in European Neuropsychopharmacology. 2019;29(6):S533-S534.
doi:10.1016/j.euroneuro.2019.09.824 .

Milosavljević, Filip, Bukvić, Nikola, Pešić, Vesna, Molden, Espen, Ingelman-Sundberg, Magnus, Jukić, Marin, "Quantification of antidepressant and antipsychotic exposure increase caused by CYP2C19 and CYP2D6 intermediate and poor metabolizer status by meta-analysis" in European Neuropsychopharmacology, 29, no. 6 (2019):S533-S534,
https://doi.org/10.1016/j.euroneuro.2019.09.824 . .

TY  - CONF
AU  - Milosavljević, Filip
AU  - Vučić, M.
AU  - Manojlović, Marina
AU  - Ašujić, N.
AU  - Batinić, Bojan
AU  - Novalen, M.
AU  - Miksys, S.
AU  - Tyndale, R.F.
AU  - Ingelman-Sundberg, Magnus
AU  - Pešić, Vesna
AU  - Jukić, Marin
PY  - 2019
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3297
PB  - Elsevier Science BV, Amsterdam
C3  - European Neuropsychopharmacology
T1  - Transgenic mouse, carrier of human CYP2C19 gene, as an animal model for hyperdopaminergism-induced hyperkinesia
VL  - 29
IS  - Supplement 2
SP  - S672
EP  - S673
DO  - 10.1016/j.euroneuro.2019.01.056
ER  - 

@conference{
author = "Milosavljević, Filip and Vučić, M. and Manojlović, Marina and Ašujić, N. and Batinić, Bojan and Novalen, M. and Miksys, S. and Tyndale, R.F. and Ingelman-Sundberg, Magnus and Pešić, Vesna and Jukić, Marin",
year = "2019",
publisher = "Elsevier Science BV, Amsterdam",
journal = "European Neuropsychopharmacology",
title = "Transgenic mouse, carrier of human CYP2C19 gene, as an animal model for hyperdopaminergism-induced hyperkinesia",
volume = "29",
number = "Supplement 2",
pages = "S672-S673",
doi = "10.1016/j.euroneuro.2019.01.056"
}

Milosavljević, F., Vučić, M., Manojlović, M., Ašujić, N., Batinić, B., Novalen, M., Miksys, S., Tyndale, R.F., Ingelman-Sundberg, M., Pešić, V.,& Jukić, M.. (2019). Transgenic mouse, carrier of human CYP2C19 gene, as an animal model for hyperdopaminergism-induced hyperkinesia. in European Neuropsychopharmacology
Elsevier Science BV, Amsterdam., 29(Supplement 2), S672-S673.
https://doi.org/10.1016/j.euroneuro.2019.01.056

Milosavljević F, Vučić M, Manojlović M, Ašujić N, Batinić B, Novalen M, Miksys S, Tyndale R, Ingelman-Sundberg M, Pešić V, Jukić M. Transgenic mouse, carrier of human CYP2C19 gene, as an animal model for hyperdopaminergism-induced hyperkinesia. in European Neuropsychopharmacology. 2019;29(Supplement 2):S672-S673.
doi:10.1016/j.euroneuro.2019.01.056 .

Milosavljević, Filip, Vučić, M., Manojlović, Marina, Ašujić, N., Batinić, Bojan, Novalen, M., Miksys, S., Tyndale, R.F., Ingelman-Sundberg, Magnus, Pešić, Vesna, Jukić, Marin, "Transgenic mouse, carrier of human CYP2C19 gene, as an animal model for hyperdopaminergism-induced hyperkinesia" in European Neuropsychopharmacology, 29, no. Supplement 2 (2019):S672-S673,
https://doi.org/10.1016/j.euroneuro.2019.01.056 . .

TY  - JOUR
AU  - Durić, Vedrana
AU  - Batinić, Bojan
AU  - Petrović, Jelena
AU  - Stanić, Dušanka
AU  - Bulat, Zorica
AU  - Pešić, Vesna
PY  - 2018
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3172
AB  - Although a magnesium-mediated attenuation of memory deficits was reported in animal models of ageing and traumatic brain injury, a possible memory enhancement in healthy subjects has not been investigated yet. We used novel object recognition test (NORT) to examine the effects of acute (30 mg/kg) and chronic (50 mg/kg, 28 days) Mg-sulfate treatment on the long-term memory (LTM) in healthy adult male rats, and to test the sustainability of magnesium effects in the models of acute and chronic (21 days) ACTH administration (10 mu g/animal), mimicking the stress- and depression-like conditions. A single dose of Mg-sulfate enhanced the LTM retrieval in the 24 h inter-trial NORT protocol, in healthy, as well as in rats acutely treated with ACTH. Memory enhancement was also detected after 4-week long Mg-sulfate intake, in both healthy and rats chronically treated with ACTH. While the present findings on procognitive effects of chronic Mg-sulfate treatment corroborate with those from studies on the therapeutic potential of Mg-threonate, the current study is the first to report on memory enhancement induced by a single dose of magnesium.
PB  - John Libbey Eurotext Ltd, Montrouge
T2  - Magnesium Research
T1  - A single dose of magnesium, as well as chronic administration, enhances long-term memory in novel object recognition test, in healthy and ACTH-treated rats
VL  - 31
IS  - 1
SP  - 24
EP  - 32
DO  - 10.1684/mrh.2018.0435
ER  - 

@article{
author = "Durić, Vedrana and Batinić, Bojan and Petrović, Jelena and Stanić, Dušanka and Bulat, Zorica and Pešić, Vesna",
year = "2018",
abstract = "Although a magnesium-mediated attenuation of memory deficits was reported in animal models of ageing and traumatic brain injury, a possible memory enhancement in healthy subjects has not been investigated yet. We used novel object recognition test (NORT) to examine the effects of acute (30 mg/kg) and chronic (50 mg/kg, 28 days) Mg-sulfate treatment on the long-term memory (LTM) in healthy adult male rats, and to test the sustainability of magnesium effects in the models of acute and chronic (21 days) ACTH administration (10 mu g/animal), mimicking the stress- and depression-like conditions. A single dose of Mg-sulfate enhanced the LTM retrieval in the 24 h inter-trial NORT protocol, in healthy, as well as in rats acutely treated with ACTH. Memory enhancement was also detected after 4-week long Mg-sulfate intake, in both healthy and rats chronically treated with ACTH. While the present findings on procognitive effects of chronic Mg-sulfate treatment corroborate with those from studies on the therapeutic potential of Mg-threonate, the current study is the first to report on memory enhancement induced by a single dose of magnesium.",
publisher = "John Libbey Eurotext Ltd, Montrouge",
journal = "Magnesium Research",
title = "A single dose of magnesium, as well as chronic administration, enhances long-term memory in novel object recognition test, in healthy and ACTH-treated rats",
volume = "31",
number = "1",
pages = "24-32",
doi = "10.1684/mrh.2018.0435"
}

Durić, V., Batinić, B., Petrović, J., Stanić, D., Bulat, Z.,& Pešić, V.. (2018). A single dose of magnesium, as well as chronic administration, enhances long-term memory in novel object recognition test, in healthy and ACTH-treated rats. in Magnesium Research
John Libbey Eurotext Ltd, Montrouge., 31(1), 24-32.
https://doi.org/10.1684/mrh.2018.0435

Durić V, Batinić B, Petrović J, Stanić D, Bulat Z, Pešić V. A single dose of magnesium, as well as chronic administration, enhances long-term memory in novel object recognition test, in healthy and ACTH-treated rats. in Magnesium Research. 2018;31(1):24-32.
doi:10.1684/mrh.2018.0435 .

Durić, Vedrana, Batinić, Bojan, Petrović, Jelena, Stanić, Dušanka, Bulat, Zorica, Pešić, Vesna, "A single dose of magnesium, as well as chronic administration, enhances long-term memory in novel object recognition test, in healthy and ACTH-treated rats" in Magnesium Research, 31, no. 1 (2018):24-32,
https://doi.org/10.1684/mrh.2018.0435 . .

TY  - JOUR
AU  - Petrović, Jelena
AU  - Stanić, Dušanka
AU  - Bulat, Zorica
AU  - Puskas, Nela
AU  - Labudović-Borović, Milica
AU  - Batinić, Bojan
AU  - Mirković, Duško
AU  - Ignjatović, Svetlana
AU  - Pešić, Vesna
PY  - 2018
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3042
AB  - Magnesium (Mg), is not only a modulator of the glutamatergic NMDA receptors' affinity, it also prevents HPA axis hyperactivity, thus possibly being implicated in neurobiological features of mood disorders. Further uncovering of molecular mechanisms underlying magnesium's proposed effects is needed due to the recent shift in research of treatment resistant depression (TRD) towards glutamatergic pathways. Here, we applied Mg via drinking water for 28 days (50 mg/kg/day), in ACTH-treated rats, an established animal model of depression resistant to tricyclic antidepressants. Using this model in male rats we measured (1) changes in hippocampal neurogenesis and behavioral alterations, (2) adrenal hormones response to acute stress challenge and (3) levels of biometals involved in regulation of monoamines turnover in rat prefrontal cortex. Our results support beneficial behavioral impact of Mg in TRD model together with increased hippocampal neurogenesis and BDNF expression. Furthermore, Mg prevented ACTH-induced disruption in HPA axis function, by normalizing the levels of plasma ACTH, corticosterone and interleukin-6, and by increasing the peripheral release of adrenaline, noradrenaline and serotonin after the acute stress challenge. Finally, the influence on copper/zinc ratio suggested probable magnesium's involvement in monoamine turnover in PFC. Our findings provide further insights into the possible pathways implicated in the behavioral modulation effects of Mg, as well as its central and peripheral effects in ACTH-induced TRD model. Thus, further investigation of molecular signaling related to the glutamatergic transmission and role of Mg, could reveal prospects to novel treatment strategies that could be of particular importance for patients suffering from TRD.
PB  - Academic Press Inc Elsevier Science, San Diego
T2  - Hormones and Behavior
T1  - Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration
VL  - 105
SP  - 1
EP  - 10
DO  - 10.1016/j.yhbeh.2018.07.003
ER  - 

@article{
author = "Petrović, Jelena and Stanić, Dušanka and Bulat, Zorica and Puskas, Nela and Labudović-Borović, Milica and Batinić, Bojan and Mirković, Duško and Ignjatović, Svetlana and Pešić, Vesna",
year = "2018",
abstract = "Magnesium (Mg), is not only a modulator of the glutamatergic NMDA receptors' affinity, it also prevents HPA axis hyperactivity, thus possibly being implicated in neurobiological features of mood disorders. Further uncovering of molecular mechanisms underlying magnesium's proposed effects is needed due to the recent shift in research of treatment resistant depression (TRD) towards glutamatergic pathways. Here, we applied Mg via drinking water for 28 days (50 mg/kg/day), in ACTH-treated rats, an established animal model of depression resistant to tricyclic antidepressants. Using this model in male rats we measured (1) changes in hippocampal neurogenesis and behavioral alterations, (2) adrenal hormones response to acute stress challenge and (3) levels of biometals involved in regulation of monoamines turnover in rat prefrontal cortex. Our results support beneficial behavioral impact of Mg in TRD model together with increased hippocampal neurogenesis and BDNF expression. Furthermore, Mg prevented ACTH-induced disruption in HPA axis function, by normalizing the levels of plasma ACTH, corticosterone and interleukin-6, and by increasing the peripheral release of adrenaline, noradrenaline and serotonin after the acute stress challenge. Finally, the influence on copper/zinc ratio suggested probable magnesium's involvement in monoamine turnover in PFC. Our findings provide further insights into the possible pathways implicated in the behavioral modulation effects of Mg, as well as its central and peripheral effects in ACTH-induced TRD model. Thus, further investigation of molecular signaling related to the glutamatergic transmission and role of Mg, could reveal prospects to novel treatment strategies that could be of particular importance for patients suffering from TRD.",
publisher = "Academic Press Inc Elsevier Science, San Diego",
journal = "Hormones and Behavior",
title = "Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration",
volume = "105",
pages = "1-10",
doi = "10.1016/j.yhbeh.2018.07.003"
}

Petrović, J., Stanić, D., Bulat, Z., Puskas, N., Labudović-Borović, M., Batinić, B., Mirković, D., Ignjatović, S.,& Pešić, V.. (2018). Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration. in Hormones and Behavior
Academic Press Inc Elsevier Science, San Diego., 105, 1-10.
https://doi.org/10.1016/j.yhbeh.2018.07.003

Petrović J, Stanić D, Bulat Z, Puskas N, Labudović-Borović M, Batinić B, Mirković D, Ignjatović S, Pešić V. Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration. in Hormones and Behavior. 2018;105:1-10.
doi:10.1016/j.yhbeh.2018.07.003 .

Petrović, Jelena, Stanić, Dušanka, Bulat, Zorica, Puskas, Nela, Labudović-Borović, Milica, Batinić, Bojan, Mirković, Duško, Ignjatović, Svetlana, Pešić, Vesna, "Acth-induced model of depression resistant to tricyclic antidepressants: Neuroendocrine and behavioral changes and influence of long-term magnesium administration" in Hormones and Behavior, 105 (2018):1-10,
https://doi.org/10.1016/j.yhbeh.2018.07.003 . .

TY  - JOUR
AU  - Miljević, Čedo D.
AU  - Nikolić-Kokić, Aleksandra
AU  - Blagojević, Duško
AU  - Milovanović, Maja
AU  - Munjiza, Ana
AU  - Jukić, Marin
AU  - Pešić, Vesna
AU  - Lecić-Tosevski, Dušica
AU  - Spasić, Mihajlo B.
PY  - 2018
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3058
AB  - To determine the relationship between alterations in the activity of the enzymes participating in antioxidative defense system and neurological soft signs (NSS) in schizophrenic patients with the first episode psychosis (S-FE, n = 19), patients in relapse (S-R, n = 46), and healthy controls (HC, n = 20). NSS intensity and enzymatic plasma activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) were compared between S-FE, S-R and HC subjects and a follow-up correlation analyses between the enzyme activities and NSS intensity was performed. NSS intensity was increased four times in schizophrenic patients compared with healthy controls. Activities of SOD and CAT were 40% decreased in S-FE and these reductions were ameliorated by antipsychotic treatment. GPX activity was 20% decreased in both patient groups compared with controls. A negative correlation between NSS intensity and GPX activity was specifically found in the S-FE patients. The data in this report argue that a reduction of GPX activity might be one of the causes for the emergence of NSS at the onset of schizophrenia, and provide the evidence that antipsychotic therapy can attenuate activity reductions of SOD and CAT, but not the activity reduction of GPX and the intensity of NSS.
PB  - Elsevier Ireland Ltd, Clare
T2  - Psychoneuroendocrinology
T1  - Association between neurological soft signs and antioxidant enzyme activity in schizophrenic patients
VL  - 269
SP  - 746
EP  - 752
DO  - 10.1016/j.psychres.2018.09.009
ER  - 

@article{
author = "Miljević, Čedo D. and Nikolić-Kokić, Aleksandra and Blagojević, Duško and Milovanović, Maja and Munjiza, Ana and Jukić, Marin and Pešić, Vesna and Lecić-Tosevski, Dušica and Spasić, Mihajlo B.",
year = "2018",
abstract = "To determine the relationship between alterations in the activity of the enzymes participating in antioxidative defense system and neurological soft signs (NSS) in schizophrenic patients with the first episode psychosis (S-FE, n = 19), patients in relapse (S-R, n = 46), and healthy controls (HC, n = 20). NSS intensity and enzymatic plasma activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) were compared between S-FE, S-R and HC subjects and a follow-up correlation analyses between the enzyme activities and NSS intensity was performed. NSS intensity was increased four times in schizophrenic patients compared with healthy controls. Activities of SOD and CAT were 40% decreased in S-FE and these reductions were ameliorated by antipsychotic treatment. GPX activity was 20% decreased in both patient groups compared with controls. A negative correlation between NSS intensity and GPX activity was specifically found in the S-FE patients. The data in this report argue that a reduction of GPX activity might be one of the causes for the emergence of NSS at the onset of schizophrenia, and provide the evidence that antipsychotic therapy can attenuate activity reductions of SOD and CAT, but not the activity reduction of GPX and the intensity of NSS.",
publisher = "Elsevier Ireland Ltd, Clare",
journal = "Psychoneuroendocrinology",
title = "Association between neurological soft signs and antioxidant enzyme activity in schizophrenic patients",
volume = "269",
pages = "746-752",
doi = "10.1016/j.psychres.2018.09.009"
}

Miljević, Č. D., Nikolić-Kokić, A., Blagojević, D., Milovanović, M., Munjiza, A., Jukić, M., Pešić, V., Lecić-Tosevski, D.,& Spasić, M. B.. (2018). Association between neurological soft signs and antioxidant enzyme activity in schizophrenic patients. in Psychoneuroendocrinology
Elsevier Ireland Ltd, Clare., 269, 746-752.
https://doi.org/10.1016/j.psychres.2018.09.009

Miljević ČD, Nikolić-Kokić A, Blagojević D, Milovanović M, Munjiza A, Jukić M, Pešić V, Lecić-Tosevski D, Spasić MB. Association between neurological soft signs and antioxidant enzyme activity in schizophrenic patients. in Psychoneuroendocrinology. 2018;269:746-752.
doi:10.1016/j.psychres.2018.09.009 .

Miljević, Čedo D., Nikolić-Kokić, Aleksandra, Blagojević, Duško, Milovanović, Maja, Munjiza, Ana, Jukić, Marin, Pešić, Vesna, Lecić-Tosevski, Dušica, Spasić, Mihajlo B., "Association between neurological soft signs and antioxidant enzyme activity in schizophrenic patients" in Psychoneuroendocrinology, 269 (2018):746-752,
https://doi.org/10.1016/j.psychres.2018.09.009 . .

TY  - JOUR
AU  - Milutinović, Katarina
AU  - Stojiljković, Stanimir
AU  - Ćuk, Jelena
AU  - Lasica, Ratko
AU  - Miosavljević, Andrej
AU  - Cvetković, Dimitrije
AU  - Trajković, Aleksandra
AU  - Pešić, Vesna
AU  - Arena, Ross
AU  - Popović, Dejana
PY  - 2018
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3111
AB  - The athlete's heart is a set of morphological and functional characteristics that develop over time due to sports training. These adaptive changes result in increase in cardiac work efficiency and economy. They are manidested as cardiac muscle hypertrophy and dilation, with accompanying angiogenesis and slower heart rate, that are influenced by variable regulatory systems and genetic predisposition. The problem of sudden cardiac death in athletes, which persists despite numerous activities aimed at prevention, creates the need for a better definition of the athlete's heart, especially in terms of its differentiation from certain pathological conditions. This is of particular importance in the context of cardiac electrical activity. Right heart adaptations, hormonal regulatory mechanisms and the effects of nonphysiological adaptations during training, that may lead to pathologic alterations direction, are all relevant in the investigation of adverse cardiac events in athletes. In order to prevent sudden cardiac death in athletes, it is necessary to examine competitive athletes as well as apparently health individuals who recreationally exercise at a high volume. There are guidelines for mass screening and individual examinations, for all age groups and both genders, as well as for public service staff who require intense physical activity during their occupation. Both American and European recommendations require a detailed anamnesis and physical examination, whereas European, apart from that, require initial electrocardiography. The implementation of additional tests is necessary if the existence of any underlying pathophysiologic process is suspected. Checks should be performed before engaging in sports activities, as well as during training and competition periods.
AB  - Sportsko srce predstavlja efekat morfoloških i funkcionalnih adaptacija srca koje se razvijaju tokom vremena, pod uticajem sportskog treninga. Promene na srcu kod sportista za posledicu imaju promenu efikasnosti i ekonomičnosti srčanog rada. Manifestuju se hipertrofijom i dilatacijom srca, sa pratećom angiogenezom i usporenim srčanim radom, procesima koji su pod kontrolom različitih regulatornih sistema i genetske predispozicije. Problem iznenadne srčane smrti u sportu, čija se incidenca ne smanjuje uprkos brojnim aktivnostima koje se sprovode u cilju njene prevencije, nameće potrebu boljeg definisanja sportskog srca, naročito u smislu njegovog razlikovanja od pojedinih patoloških stanja. Kod izvesnog broja sportista uočavaju se promene električne aktivnosti, te je i u tom smislu potrebno razlikovati zdravo od bolesnog srca. Poslednjih godina posebno je u fokusu definisanje adaptivnih promena desnog srca. Dodatno, postoje nova saznanja o hormonskoj regulaciji adaptivnih promena srca sportista, a istražuju se i efekti nefizioloških manipulacija u trenažnom procesu koji mogu 'skrenuti' fiziološke procese u patološkom pravcu. U cilju prevencije iznenadne srčane smrti, neophodno je redovno pregledanje kako sportista, tako i fizički aktivnog dela populacije. Aktuelne preporuke daju smernice za masovne skrininge i individualne preglede sportista, za sve starosne grupe oba pola, kao i pripadnike javnih službi koje u opisu posla imaju intenzivne fizičke napore. Dok američke preporuke zahtevaju samo detaljnu anamnezu i fizikalni pregled, evropske preporuke zahtevaju i inicijalnu elektrokardiografiju. I evropske i američke preporuke zahtevaju sprovođenje dodatnih ispitivanja kod sumnje na postojanje bilo kakvog oboljenja. Ove preglede bi trebalo obavljati pre početka trenažnog procesa, kao i tokom perioda treniranja i takmičenja.
PB  - Univerzitet u Beogradu - Fakultet sporta i fizičkog vaspitanja, Beograd
T2  - Fizička kultura
T1  - Athlete's heart
T1  - Corazon de deportista
T1  - Sportsko srce
VL  - 72
IS  - 2
SP  - 139
EP  - 147
DO  - 10.5937/fizkul1802139M
ER  - 

@article{
author = "Milutinović, Katarina and Stojiljković, Stanimir and Ćuk, Jelena and Lasica, Ratko and Miosavljević, Andrej and Cvetković, Dimitrije and Trajković, Aleksandra and Pešić, Vesna and Arena, Ross and Popović, Dejana",
year = "2018",
abstract = "The athlete's heart is a set of morphological and functional characteristics that develop over time due to sports training. These adaptive changes result in increase in cardiac work efficiency and economy. They are manidested as cardiac muscle hypertrophy and dilation, with accompanying angiogenesis and slower heart rate, that are influenced by variable regulatory systems and genetic predisposition. The problem of sudden cardiac death in athletes, which persists despite numerous activities aimed at prevention, creates the need for a better definition of the athlete's heart, especially in terms of its differentiation from certain pathological conditions. This is of particular importance in the context of cardiac electrical activity. Right heart adaptations, hormonal regulatory mechanisms and the effects of nonphysiological adaptations during training, that may lead to pathologic alterations direction, are all relevant in the investigation of adverse cardiac events in athletes. In order to prevent sudden cardiac death in athletes, it is necessary to examine competitive athletes as well as apparently health individuals who recreationally exercise at a high volume. There are guidelines for mass screening and individual examinations, for all age groups and both genders, as well as for public service staff who require intense physical activity during their occupation. Both American and European recommendations require a detailed anamnesis and physical examination, whereas European, apart from that, require initial electrocardiography. The implementation of additional tests is necessary if the existence of any underlying pathophysiologic process is suspected. Checks should be performed before engaging in sports activities, as well as during training and competition periods., Sportsko srce predstavlja efekat morfoloških i funkcionalnih adaptacija srca koje se razvijaju tokom vremena, pod uticajem sportskog treninga. Promene na srcu kod sportista za posledicu imaju promenu efikasnosti i ekonomičnosti srčanog rada. Manifestuju se hipertrofijom i dilatacijom srca, sa pratećom angiogenezom i usporenim srčanim radom, procesima koji su pod kontrolom različitih regulatornih sistema i genetske predispozicije. Problem iznenadne srčane smrti u sportu, čija se incidenca ne smanjuje uprkos brojnim aktivnostima koje se sprovode u cilju njene prevencije, nameće potrebu boljeg definisanja sportskog srca, naročito u smislu njegovog razlikovanja od pojedinih patoloških stanja. Kod izvesnog broja sportista uočavaju se promene električne aktivnosti, te je i u tom smislu potrebno razlikovati zdravo od bolesnog srca. Poslednjih godina posebno je u fokusu definisanje adaptivnih promena desnog srca. Dodatno, postoje nova saznanja o hormonskoj regulaciji adaptivnih promena srca sportista, a istražuju se i efekti nefizioloških manipulacija u trenažnom procesu koji mogu 'skrenuti' fiziološke procese u patološkom pravcu. U cilju prevencije iznenadne srčane smrti, neophodno je redovno pregledanje kako sportista, tako i fizički aktivnog dela populacije. Aktuelne preporuke daju smernice za masovne skrininge i individualne preglede sportista, za sve starosne grupe oba pola, kao i pripadnike javnih službi koje u opisu posla imaju intenzivne fizičke napore. Dok američke preporuke zahtevaju samo detaljnu anamnezu i fizikalni pregled, evropske preporuke zahtevaju i inicijalnu elektrokardiografiju. I evropske i američke preporuke zahtevaju sprovođenje dodatnih ispitivanja kod sumnje na postojanje bilo kakvog oboljenja. Ove preglede bi trebalo obavljati pre početka trenažnog procesa, kao i tokom perioda treniranja i takmičenja.",
publisher = "Univerzitet u Beogradu - Fakultet sporta i fizičkog vaspitanja, Beograd",
journal = "Fizička kultura",
title = "Athlete's heart, Corazon de deportista, Sportsko srce",
volume = "72",
number = "2",
pages = "139-147",
doi = "10.5937/fizkul1802139M"
}

Milutinović, K., Stojiljković, S., Ćuk, J., Lasica, R., Miosavljević, A., Cvetković, D., Trajković, A., Pešić, V., Arena, R.,& Popović, D.. (2018). Athlete's heart. in Fizička kultura
Univerzitet u Beogradu - Fakultet sporta i fizičkog vaspitanja, Beograd., 72(2), 139-147.
https://doi.org/10.5937/fizkul1802139M

Milutinović K, Stojiljković S, Ćuk J, Lasica R, Miosavljević A, Cvetković D, Trajković A, Pešić V, Arena R, Popović D. Athlete's heart. in Fizička kultura. 2018;72(2):139-147.
doi:10.5937/fizkul1802139M .

Milutinović, Katarina, Stojiljković, Stanimir, Ćuk, Jelena, Lasica, Ratko, Miosavljević, Andrej, Cvetković, Dimitrije, Trajković, Aleksandra, Pešić, Vesna, Arena, Ross, Popović, Dejana, "Athlete's heart" in Fizička kultura, 72, no. 2 (2018):139-147,
https://doi.org/10.5937/fizkul1802139M . .

TY  - JOUR
AU  - Ćuk, Jelena
AU  - Stojiljković, Stanimir
AU  - Milutinović, Katarina
AU  - Cvetković, Dimitrije
AU  - Pešić, Vesna
AU  - Arena, Ross
AU  - Popović, Dejana
PY  - 2018
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3102
AB  - The athlete's heart is an exercise-induced cardiac remodeling phenomenon, which is individual and depends on the intensity, duration and frequency of training, as well as genetic factors. Cardiovascular screening prior to participation in sports activities, is a systematic practice of medical evaluation in the athlete population. The current US recommendations for the screening of cardiovascular abnormalities in high school and university athletes at all levels of performance were initially put forther by the American Heart Association in 2007. These recommendations consist of 12 points, factoring personal and family history data, as well as physical examination. On the other hand, European recommendations suggest the importance of non-invasive diagnostic methods, such as the 12-lead ECG, which should be carried out in combination with a history and physical examination. According to the European Association for Cardiovascular Imaging, standard echocardiography is the first line approach to differentiate an athlete's heart from pathological left ventricular hypertrophy. Updated 'Seattle criteria' from 2017. include criteria for assessing abnormalities in the electrocardiogram of athletes and their differentiation from the adaptive electrophysiological changes, which do not require further evaluation. Since sudden cardiac death during sport activities remains a major concern and, as such, it is imperative for the physician to diagnose unrecognized pathological conditions in athletes. Following current expert consensus recommendations on this topic helps to prevent untoward events during physical activity in those who are found to be at elevated risk.
AB  - Atletsko srce je fenomen remodelovanja srčanog mišića, koje je nastalo usled fizičke aktivnosti, a čiji stepen zavisi od intenziteta, trajanja, učestalosti treniranja, individualnih osobina i genetskih faktora. Aktuelne američke preporuke za skrining kardiovaskularnih abnormalnosti među sportistima srednjoškolcima i studentima svih nivoa utreniranosti, inicijalno su bile postavljene od strane Američkog udruženja kardiologa 2007. godine. Ove preporuke čini 12 tačaka i podrazumevaju podatke iz lične i porodične istorije bolesti, kao i fizičkog pregleda. S druge strane, evropske preporuke sugerišu na značaj neinvazivnih dijagnostičkih metoda, kao što je 12-kanalni EKG, čiji rezultati bi trebali biti razmatrani udruženo sa istorijom bolesti i fizičkim pregledom. Prema Evropskom udruženju za kardiovakularni imidžing, standardna ehokardiografija je prva dijagnostička metoda diferencijacije sportskog srca od patološke hipertrofije leve komore. Godine 2012, Američko udruženje za sportsku medicine je definisalo kriterijume, koji su osveženi 2017. godine, za utvrđivanje abnormalnosti u elektrokardiogramu sportista i njihovu diferencijaciju od adaptivnih elektrofizoloških promena, koje ne zahtevaju dalju evaluaciju. S obzirom na to da iznenadna srčana smrt u sportu zahteva veliku pažnju, neophodno je da lekari budu edukovani da dijagnostikuju neprepoznata patološka stanja kod sportista. Praćenje aktuelnih preporuka koje se bave ovim problemom doprinosi prevenciji neželjenih događaja u sportu i kod osoba koje su iz drugih razloga izložene velikim fizičkim naporima.
PB  - Savez farmaceutskih udruženja Srbije, Beograd
T2  - Arhiv za farmaciju
T1  - The athlete's heart: Modern diagnostic approach
T1  - Sportsko srce - savremeni dijagnostički pristup
VL  - 68
IS  - 4
SP  - 900
EP  - 910
DO  - 10.5937/ArhFarm1804900C
ER  - 

@article{
author = "Ćuk, Jelena and Stojiljković, Stanimir and Milutinović, Katarina and Cvetković, Dimitrije and Pešić, Vesna and Arena, Ross and Popović, Dejana",
year = "2018",
abstract = "The athlete's heart is an exercise-induced cardiac remodeling phenomenon, which is individual and depends on the intensity, duration and frequency of training, as well as genetic factors. Cardiovascular screening prior to participation in sports activities, is a systematic practice of medical evaluation in the athlete population. The current US recommendations for the screening of cardiovascular abnormalities in high school and university athletes at all levels of performance were initially put forther by the American Heart Association in 2007. These recommendations consist of 12 points, factoring personal and family history data, as well as physical examination. On the other hand, European recommendations suggest the importance of non-invasive diagnostic methods, such as the 12-lead ECG, which should be carried out in combination with a history and physical examination. According to the European Association for Cardiovascular Imaging, standard echocardiography is the first line approach to differentiate an athlete's heart from pathological left ventricular hypertrophy. Updated 'Seattle criteria' from 2017. include criteria for assessing abnormalities in the electrocardiogram of athletes and their differentiation from the adaptive electrophysiological changes, which do not require further evaluation. Since sudden cardiac death during sport activities remains a major concern and, as such, it is imperative for the physician to diagnose unrecognized pathological conditions in athletes. Following current expert consensus recommendations on this topic helps to prevent untoward events during physical activity in those who are found to be at elevated risk., Atletsko srce je fenomen remodelovanja srčanog mišića, koje je nastalo usled fizičke aktivnosti, a čiji stepen zavisi od intenziteta, trajanja, učestalosti treniranja, individualnih osobina i genetskih faktora. Aktuelne američke preporuke za skrining kardiovaskularnih abnormalnosti među sportistima srednjoškolcima i studentima svih nivoa utreniranosti, inicijalno su bile postavljene od strane Američkog udruženja kardiologa 2007. godine. Ove preporuke čini 12 tačaka i podrazumevaju podatke iz lične i porodične istorije bolesti, kao i fizičkog pregleda. S druge strane, evropske preporuke sugerišu na značaj neinvazivnih dijagnostičkih metoda, kao što je 12-kanalni EKG, čiji rezultati bi trebali biti razmatrani udruženo sa istorijom bolesti i fizičkim pregledom. Prema Evropskom udruženju za kardiovakularni imidžing, standardna ehokardiografija je prva dijagnostička metoda diferencijacije sportskog srca od patološke hipertrofije leve komore. Godine 2012, Američko udruženje za sportsku medicine je definisalo kriterijume, koji su osveženi 2017. godine, za utvrđivanje abnormalnosti u elektrokardiogramu sportista i njihovu diferencijaciju od adaptivnih elektrofizoloških promena, koje ne zahtevaju dalju evaluaciju. S obzirom na to da iznenadna srčana smrt u sportu zahteva veliku pažnju, neophodno je da lekari budu edukovani da dijagnostikuju neprepoznata patološka stanja kod sportista. Praćenje aktuelnih preporuka koje se bave ovim problemom doprinosi prevenciji neželjenih događaja u sportu i kod osoba koje su iz drugih razloga izložene velikim fizičkim naporima.",
publisher = "Savez farmaceutskih udruženja Srbije, Beograd",
journal = "Arhiv za farmaciju",
title = "The athlete's heart: Modern diagnostic approach, Sportsko srce - savremeni dijagnostički pristup",
volume = "68",
number = "4",
pages = "900-910",
doi = "10.5937/ArhFarm1804900C"
}

Ćuk, J., Stojiljković, S., Milutinović, K., Cvetković, D., Pešić, V., Arena, R.,& Popović, D.. (2018). The athlete's heart: Modern diagnostic approach. in Arhiv za farmaciju
Savez farmaceutskih udruženja Srbije, Beograd., 68(4), 900-910.
https://doi.org/10.5937/ArhFarm1804900C

Ćuk J, Stojiljković S, Milutinović K, Cvetković D, Pešić V, Arena R, Popović D. The athlete's heart: Modern diagnostic approach. in Arhiv za farmaciju. 2018;68(4):900-910.
doi:10.5937/ArhFarm1804900C .

Ćuk, Jelena, Stojiljković, Stanimir, Milutinović, Katarina, Cvetković, Dimitrije, Pešić, Vesna, Arena, Ross, Popović, Dejana, "The athlete's heart: Modern diagnostic approach" in Arhiv za farmaciju, 68, no. 4 (2018):900-910,
https://doi.org/10.5937/ArhFarm1804900C . .

TY  - CONF
AU  - Petrović, Jelena
AU  - Labudović-Borović, Milica
AU  - Puškaš, Nela
AU  - Stanić, Dušanka
AU  - Batinić, Bojan
AU  - Plećaš-Solarović, Bosiljka
AU  - Pešić, Vesna
PY  - 2017
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/2894
PB  - Elsevier Science BV, Amsterdam
C3  - European Neuropsychopharmacology
T1  - Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats
VL  - 27
IS  - Supplement 4
SP  - S765
EP  - S766
DO  - 10.1016/S0924-977X(17)31398-6
ER  - 

@conference{
author = "Petrović, Jelena and Labudović-Borović, Milica and Puškaš, Nela and Stanić, Dušanka and Batinić, Bojan and Plećaš-Solarović, Bosiljka and Pešić, Vesna",
year = "2017",
publisher = "Elsevier Science BV, Amsterdam",
journal = "European Neuropsychopharmacology",
title = "Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats",
volume = "27",
number = "Supplement 4",
pages = "S765-S766",
doi = "10.1016/S0924-977X(17)31398-6"
}

Petrović, J., Labudović-Borović, M., Puškaš, N., Stanić, D., Batinić, B., Plećaš-Solarović, B.,& Pešić, V.. (2017). Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats. in European Neuropsychopharmacology
Elsevier Science BV, Amsterdam., 27(Supplement 4), S765-S766.
https://doi.org/10.1016/S0924-977X(17)31398-6

Petrović J, Labudović-Borović M, Puškaš N, Stanić D, Batinić B, Plećaš-Solarović B, Pešić V. Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats. in European Neuropsychopharmacology. 2017;27(Supplement 4):S765-S766.
doi:10.1016/S0924-977X(17)31398-6 .

Petrović, Jelena, Labudović-Borović, Milica, Puškaš, Nela, Stanić, Dušanka, Batinić, Bojan, Plećaš-Solarović, Bosiljka, Pešić, Vesna, "Chronic magnesium supplementation increases hippocampal neurogenesis and decreases proliferation in myocardium in ACTH-treated rats" in European Neuropsychopharmacology, 27, no. Supplement 4 (2017):S765-S766,
https://doi.org/10.1016/S0924-977X(17)31398-6 . .