TY  - JOUR
AU  - Bjørklund, Geir
AU  - Buha-Đorđević, Aleksandra
AU  - Hamdan, Halla
AU  - Wallace, David R.
AU  - Peana, Massimiliano
PY  - 2024
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/5443
AB  - Autoimmunity is a multifaceted disorder influenced by both genetic and environmental factors, and metal exposure has been implicated as a potential catalyst, especially in autoimmune diseases affecting the central nervous system. Notably, metals like mercury, lead, and aluminum exhibit well-established neurotoxic effects, yet the precise mechanisms by which they elicit autoimmune responses in susceptible individuals remain unclear. Recent studies propose that metal-induced autoimmunity may arise from direct toxic effects on immune cells and tissues, coupled with indirect impacts on the gut microbiome and the blood-brain barrier. These effects can activate self-reactive T cells, prompting the production of autoantibodies, inflammatory responses, and tissue damage. Diagnosing metal-induced autoimmunity proves challenging due to nonspecific symptoms and a lack of reliable biomarkers. Treatment typically involves chelation therapy to eliminate excess metals and immunomodulatory agents to suppress autoimmune responses. Prevention strategies include lifestyle adjustments to reduce metal exposure and avoiding occupational and environmental risks. Prognosis is generally favorable with proper treatment; however, untreated cases may lead to autoimmune disorder progression and irreversible organ damage, particularly in the brain. Future research aims to identify genetic and environmental risk factors, enhance diagnostic precision, and explore novel treatment approaches for improved prevention and management of this intricate and debilitating disease.
PB  - Elsevier B.V.
T2  - Autoimmunity Reviews
T1  - Metal-induced autoimmunity in neurological disorders: A review of current understanding and future directions
VL  - 23
IS  - 3
DO  - 10.1016/j.autrev.2023.103509
DO  - 2-s2.0-85181822086
ER  - 

@article{
author = "Bjørklund, Geir and Buha-Đorđević, Aleksandra and Hamdan, Halla and Wallace, David R. and Peana, Massimiliano",
year = "2024",
abstract = "Autoimmunity is a multifaceted disorder influenced by both genetic and environmental factors, and metal exposure has been implicated as a potential catalyst, especially in autoimmune diseases affecting the central nervous system. Notably, metals like mercury, lead, and aluminum exhibit well-established neurotoxic effects, yet the precise mechanisms by which they elicit autoimmune responses in susceptible individuals remain unclear. Recent studies propose that metal-induced autoimmunity may arise from direct toxic effects on immune cells and tissues, coupled with indirect impacts on the gut microbiome and the blood-brain barrier. These effects can activate self-reactive T cells, prompting the production of autoantibodies, inflammatory responses, and tissue damage. Diagnosing metal-induced autoimmunity proves challenging due to nonspecific symptoms and a lack of reliable biomarkers. Treatment typically involves chelation therapy to eliminate excess metals and immunomodulatory agents to suppress autoimmune responses. Prevention strategies include lifestyle adjustments to reduce metal exposure and avoiding occupational and environmental risks. Prognosis is generally favorable with proper treatment; however, untreated cases may lead to autoimmune disorder progression and irreversible organ damage, particularly in the brain. Future research aims to identify genetic and environmental risk factors, enhance diagnostic precision, and explore novel treatment approaches for improved prevention and management of this intricate and debilitating disease.",
publisher = "Elsevier B.V.",
journal = "Autoimmunity Reviews",
title = "Metal-induced autoimmunity in neurological disorders: A review of current understanding and future directions",
volume = "23",
number = "3",
doi = "10.1016/j.autrev.2023.103509, 2-s2.0-85181822086"
}

Bjørklund, G., Buha-Đorđević, A., Hamdan, H., Wallace, D. R.,& Peana, M.. (2024). Metal-induced autoimmunity in neurological disorders: A review of current understanding and future directions. in Autoimmunity Reviews
Elsevier B.V.., 23(3).
https://doi.org/10.1016/j.autrev.2023.103509

Bjørklund G, Buha-Đorđević A, Hamdan H, Wallace DR, Peana M. Metal-induced autoimmunity in neurological disorders: A review of current understanding and future directions. in Autoimmunity Reviews. 2024;23(3).
doi:10.1016/j.autrev.2023.103509 .

Bjørklund, Geir, Buha-Đorđević, Aleksandra, Hamdan, Halla, Wallace, David R., Peana, Massimiliano, "Metal-induced autoimmunity in neurological disorders: A review of current understanding and future directions" in Autoimmunity Reviews, 23, no. 3 (2024),
https://doi.org/10.1016/j.autrev.2023.103509 . .

TY  - JOUR
AU  - Wallace, David R.
AU  - Taalab, Yasmeen M.
AU  - Heinze, Sarah
AU  - Tariba Lovaković, Sarah
AU  - Pizent, Alica
AU  - Renieri, Elisavit
AU  - Tsatsakis, Aristidis
AU  - Farooqi, Ammad Ahmad
AU  - Javorac, Dragana
AU  - Anđelković, Milena
AU  - Bulat, Zorica
AU  - Antonijević, Biljana
AU  - Buha-Đorđević, Aleksandra
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3578
AB  - Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)-short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain-a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs).
PB  - MDPI
T2  - Cells
T1  - Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development
VL  - 9
IS  - 4
DO  - 10.3390/cells9040901
ER  - 

@article{
author = "Wallace, David R. and Taalab, Yasmeen M. and Heinze, Sarah and Tariba Lovaković, Sarah and Pizent, Alica and Renieri, Elisavit and Tsatsakis, Aristidis and Farooqi, Ammad Ahmad and Javorac, Dragana and Anđelković, Milena and Bulat, Zorica and Antonijević, Biljana and Buha-Đorđević, Aleksandra",
year = "2020",
abstract = "Toxic metals are extensively found in the environment, households, and workplaces and contaminate food and drinking water. The crosstalk between environmental exposure to toxic metals and human diseases has been frequently described. The toxic mechanism of action was classically viewed as the ability to dysregulate the redox status, production of inflammatory mediators and alteration of mitochondrial function. Recently, growing evidence showed that heavy metals might exert their toxicity through microRNAs (miRNA)-short, single-stranded, noncoding molecules that function as positive/negative regulators of gene expression. Aberrant alteration of the endogenous miRNA has been directly implicated in various pathophysiological conditions and signaling pathways, consequently leading to different types of cancer and human diseases. Additionally, the gene-regulatory capacity of miRNAs is particularly valuable in the brain-a complex organ with neurons demonstrating a significant ability to adapt following environmental stimuli. Accordingly, dysregulated miRNAs identified in patients suffering from neurological diseases might serve as biomarkers for the earlier diagnosis and monitoring of disease progression. This review will greatly emphasize the effect of the toxic metals on human miRNA activities and how this contributes to progression of diseases such as cancer and neurodegenerative disorders (NDDs).",
publisher = "MDPI",
journal = "Cells",
title = "Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development",
volume = "9",
number = "4",
doi = "10.3390/cells9040901"
}

Wallace, D. R., Taalab, Y. M., Heinze, S., Tariba Lovaković, S., Pizent, A., Renieri, E., Tsatsakis, A., Farooqi, A. A., Javorac, D., Anđelković, M., Bulat, Z., Antonijević, B.,& Buha-Đorđević, A.. (2020). Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development. in Cells
MDPI., 9(4).
https://doi.org/10.3390/cells9040901

Wallace DR, Taalab YM, Heinze S, Tariba Lovaković S, Pizent A, Renieri E, Tsatsakis A, Farooqi AA, Javorac D, Anđelković M, Bulat Z, Antonijević B, Buha-Đorđević A. Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development. in Cells. 2020;9(4).
doi:10.3390/cells9040901 .

Wallace, David R., Taalab, Yasmeen M., Heinze, Sarah, Tariba Lovaković, Sarah, Pizent, Alica, Renieri, Elisavit, Tsatsakis, Aristidis, Farooqi, Ammad Ahmad, Javorac, Dragana, Anđelković, Milena, Bulat, Zorica, Antonijević, Biljana, Buha-Đorđević, Aleksandra, "Toxic-Metal-Induced Alteration in miRNA Expression Profile as a Proposed Mechanism for Disease Development" in Cells, 9, no. 4 (2020),
https://doi.org/10.3390/cells9040901 . .

TY  - JOUR
AU  - Wallace, David R.
AU  - Buha-Đorđević, Aleksandra
AU  - Benton, Alexander
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3770
AB  - Nickel compounds are Group 1 carcinogens and possibly cancer-causing in the pancreas. We examined the toxicity of nickel in both 2-D and 3-D pancreatic cell cultures, to determine the LD50 for organic and  inorganic nickel  in normal and cancerous  cells. Assays with cadmium chloride  were performed to be  a comparison  to potential nickel-induced  toxicity.  Cells were exposed to twelve concentrations of NiCl2 or Ni-(Ac)2 for 48h (2-D), or six concentrations for 48 hours (3-D). There was a significant (P=0.0016) difference between HPNE and AsPC-1 LD50values after cadmium exposure, at 69.9 μM and 29.2 μM, respectively. Neither form of nickel exhibited toxicity in 2-D or 3-D cultures, but after 48h, changes in spheroid morphology were observed. The inability of Ni to reduce viable cell numbers suggests a toxic mechanism that differs from cadmium, also a Group 1 carcinogen. The cell microenvironment was not a factor in nickel toxicity with no changes in viable cells in either 2-D or 3-D cultures. These studies only examined cytotoxicity, and not genotoxicity, a potential mechanism of nickel carcinogenicity. Alterations in DNA function or the expression of apoptotic proteins/processes would take longer to manifest. Current work focuses on cellular changes following extended nickel exposure.
AB  - Uloga nikla, toksičnog metala, u nastanku karcinoma pankreasa još uvek nije u potpunosti ispitana. Cilj rada je da ispita toksičnost nikla (Ni) u 2-D i 3-D kulturi ćelija pankreasa, kako bi se utvrdila LD50 vrednost za organski i neorganski nikl u normalnim i tumorskim ćelijama. Ispitivanja su izvršena i sa kadmijumom (Cd), metalom čija je uloga u nastanku karcinoma pankreasa potvrđena u prethodnim istraživanjima, a u svrhu poređenja sa potencijalnom toksičnošću izazvanom Ni. Ćelije su bile tretirane sa 12 različitih koncentracija NiCl2 ili Ni-(Ac)2 tokom 48h (2-D), odnosno sa šest različitih koncentracija tokom 48 sati (3-D). Nijedan oblik Ni nije ispoljio toksičnost u 2-D ili 3-D kulturama, ali nakon 48h primećene su promene u sferoidnoj morfologiji. Nemogućnost Ni da smanji broj vijabilnih ćelija sugeriše mehanizam karcinogeneze različit od mehanizma koji ispoljava Cd. Ipak, da bi se uočile izmene u funkciji DNK ili izražavanju apoptotičkih proteina/procesa potrebno je duže vremena, pa su dalja istraživanja upravo fokusirana na ćelijske promene nakon produžene izloženosti nikla.
PB  - Pharmaceutical Association of Serbia
T2  - Arhiv za farmaciju
T1  - Toxicity of Organic and Inorganic Nickel in Pancreatic Cell Cultures: Comparison to Cadmium
T1  - Toksičnost organskog i neogranskog nikla u ćelijskim kulturama pankreasa: poređenje sa kadmijumom
VL  - 70
IS  - 6
SP  - 344
EP  - 359
DO  - 10.5937/arhfarm70-29277
ER  - 

@article{
author = "Wallace, David R. and Buha-Đorđević, Aleksandra and Benton, Alexander",
year = "2020",
abstract = "Nickel compounds are Group 1 carcinogens and possibly cancer-causing in the pancreas. We examined the toxicity of nickel in both 2-D and 3-D pancreatic cell cultures, to determine the LD50 for organic and  inorganic nickel  in normal and cancerous  cells. Assays with cadmium chloride  were performed to be  a comparison  to potential nickel-induced  toxicity.  Cells were exposed to twelve concentrations of NiCl2 or Ni-(Ac)2 for 48h (2-D), or six concentrations for 48 hours (3-D). There was a significant (P=0.0016) difference between HPNE and AsPC-1 LD50values after cadmium exposure, at 69.9 μM and 29.2 μM, respectively. Neither form of nickel exhibited toxicity in 2-D or 3-D cultures, but after 48h, changes in spheroid morphology were observed. The inability of Ni to reduce viable cell numbers suggests a toxic mechanism that differs from cadmium, also a Group 1 carcinogen. The cell microenvironment was not a factor in nickel toxicity with no changes in viable cells in either 2-D or 3-D cultures. These studies only examined cytotoxicity, and not genotoxicity, a potential mechanism of nickel carcinogenicity. Alterations in DNA function or the expression of apoptotic proteins/processes would take longer to manifest. Current work focuses on cellular changes following extended nickel exposure., Uloga nikla, toksičnog metala, u nastanku karcinoma pankreasa još uvek nije u potpunosti ispitana. Cilj rada je da ispita toksičnost nikla (Ni) u 2-D i 3-D kulturi ćelija pankreasa, kako bi se utvrdila LD50 vrednost za organski i neorganski nikl u normalnim i tumorskim ćelijama. Ispitivanja su izvršena i sa kadmijumom (Cd), metalom čija je uloga u nastanku karcinoma pankreasa potvrđena u prethodnim istraživanjima, a u svrhu poređenja sa potencijalnom toksičnošću izazvanom Ni. Ćelije su bile tretirane sa 12 različitih koncentracija NiCl2 ili Ni-(Ac)2 tokom 48h (2-D), odnosno sa šest različitih koncentracija tokom 48 sati (3-D). Nijedan oblik Ni nije ispoljio toksičnost u 2-D ili 3-D kulturama, ali nakon 48h primećene su promene u sferoidnoj morfologiji. Nemogućnost Ni da smanji broj vijabilnih ćelija sugeriše mehanizam karcinogeneze različit od mehanizma koji ispoljava Cd. Ipak, da bi se uočile izmene u funkciji DNK ili izražavanju apoptotičkih proteina/procesa potrebno je duže vremena, pa su dalja istraživanja upravo fokusirana na ćelijske promene nakon produžene izloženosti nikla.",
publisher = "Pharmaceutical Association of Serbia",
journal = "Arhiv za farmaciju",
title = "Toxicity of Organic and Inorganic Nickel in Pancreatic Cell Cultures: Comparison to Cadmium, Toksičnost organskog i neogranskog nikla u ćelijskim kulturama pankreasa: poređenje sa kadmijumom",
volume = "70",
number = "6",
pages = "344-359",
doi = "10.5937/arhfarm70-29277"
}

Wallace, D. R., Buha-Đorđević, A.,& Benton, A.. (2020). Toxicity of Organic and Inorganic Nickel in Pancreatic Cell Cultures: Comparison to Cadmium. in Arhiv za farmaciju
Pharmaceutical Association of Serbia., 70(6), 344-359.
https://doi.org/10.5937/arhfarm70-29277

Wallace DR, Buha-Đorđević A, Benton A. Toxicity of Organic and Inorganic Nickel in Pancreatic Cell Cultures: Comparison to Cadmium. in Arhiv za farmaciju. 2020;70(6):344-359.
doi:10.5937/arhfarm70-29277 .

Wallace, David R., Buha-Đorđević, Aleksandra, Benton, Alexander, "Toxicity of Organic and Inorganic Nickel in Pancreatic Cell Cultures: Comparison to Cadmium" in Arhiv za farmaciju, 70, no. 6 (2020):344-359,
https://doi.org/10.5937/arhfarm70-29277 . .

TY  - JOUR
AU  - Wallace, David R.
AU  - Buha-Đorđević, Aleksandra
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3532
AB  - There is a growing body of evidence that various pesticides and heavy metals are carcinogenic. If not directly, there is also evidence that shows that these compounds can participate in carcinogenesis in a passive or permissive role, facilitating other compounds from inducing tumor formation. Little evidence is available to aid in understanding the toxicity of metal-pesticide mixtures. In many instances, exposure to subclinical, or subtoxic, levels would be asymptomatic under a single-chemical exposure. But, we do not know how these compounds would act together. A synergistic or potentiating response could be highly possible. By chemically interacting with the environment, as well as each other, metal pesticide mixtures may yield unpredictable toxicity. Because we are not exposed to a single xenobiotic at a time, the importance of studying the toxicity of mixtures has never been more critical.
PB  - Elsevier B.V.
T2  - Current Opinion in Toxicology
T1  - Heavy metal and pesticide exposure: A mixture of potential toxicity and carcinogenicity
VL  - 19
SP  - 72
EP  - 79
DO  - 10.1016/j.cotox.2020.01.001
ER  - 

@article{
author = "Wallace, David R. and Buha-Đorđević, Aleksandra",
year = "2020",
abstract = "There is a growing body of evidence that various pesticides and heavy metals are carcinogenic. If not directly, there is also evidence that shows that these compounds can participate in carcinogenesis in a passive or permissive role, facilitating other compounds from inducing tumor formation. Little evidence is available to aid in understanding the toxicity of metal-pesticide mixtures. In many instances, exposure to subclinical, or subtoxic, levels would be asymptomatic under a single-chemical exposure. But, we do not know how these compounds would act together. A synergistic or potentiating response could be highly possible. By chemically interacting with the environment, as well as each other, metal pesticide mixtures may yield unpredictable toxicity. Because we are not exposed to a single xenobiotic at a time, the importance of studying the toxicity of mixtures has never been more critical.",
publisher = "Elsevier B.V.",
journal = "Current Opinion in Toxicology",
title = "Heavy metal and pesticide exposure: A mixture of potential toxicity and carcinogenicity",
volume = "19",
pages = "72-79",
doi = "10.1016/j.cotox.2020.01.001"
}

Wallace, D. R.,& Buha-Đorđević, A.. (2020). Heavy metal and pesticide exposure: A mixture of potential toxicity and carcinogenicity. in Current Opinion in Toxicology
Elsevier B.V.., 19, 72-79.
https://doi.org/10.1016/j.cotox.2020.01.001

Wallace DR, Buha-Đorđević A. Heavy metal and pesticide exposure: A mixture of potential toxicity and carcinogenicity. in Current Opinion in Toxicology. 2020;19:72-79.
doi:10.1016/j.cotox.2020.01.001 .

Wallace, David R., Buha-Đorđević, Aleksandra, "Heavy metal and pesticide exposure: A mixture of potential toxicity and carcinogenicity" in Current Opinion in Toxicology, 19 (2020):72-79,
https://doi.org/10.1016/j.cotox.2020.01.001 . .

TY  - JOUR
AU  - Varmazyari, Atefeh
AU  - Taghizadehghalehjoughi, Ali
AU  - Sevim, Cigdem
AU  - Baris, Ozlem
AU  - Eser, Gizem
AU  - Yildirim, Serkan
AU  - Hacimuftuoglu, Ahmet
AU  - Buha, Aleksandra
AU  - Wallace, David R.
AU  - Tsatsakis, Aristidis
AU  - Aschner, Michael
AU  - Mezhuev, Yaroslav
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3593
AB  - Living organisms have an innate ability to regulate the synthesis of inorganic materials, such as bones and teeth in humans. Cadmium sulfide (CdS) can be utilized as a quantum dot that functions as a unique light-emitting semiconductor nanocrystal. The increased use in CdS has led to an increased inhalation and ingestion rate of CdS by humans which requires a broader appreciation for the acute and chronic toxicity of CdS. We investigated the toxic effects of CdS on cerebellar cell cultures and rat brain. We employed a ‘green synthesis’ biosynthesis process to obtain biocompatible material that can be used in living organisms, such as Viridibacillus arenosi K64. Nanocrystal formation was initiated by adding CdCl2 (1 mM) to the cell cultures. Our in vitro results established that increased concentrations of CdS (0.1 μg/mL) lead to decreased cell viability as assessed using 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT), total antioxidant capacity (TAC), and total oxidant status (TOS). The in vivo studies showed that exposure to CdS (1 mg/kg) glial fibrillary acidic protein (GFAP) and 8-hydroxy-2' -deoxyguanosine (8-OHdG) were increased. Collectively, we describe a model system that addresses the process from the synthesis to the neurotoxicity assessment for CdS both in vitro and in vivo. These data will be beneficial in establishing a more comprehensive pathway for the understanding of quantum dot-induced neurotoxicity.
PB  - Elsevier
T2  - Toxicology Reports
T1  - Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies
VL  - 7
SP  - 637
EP  - 648
DO  - 10.1016/j.toxrep.2020.04.011
ER  - 

@article{
author = "Varmazyari, Atefeh and Taghizadehghalehjoughi, Ali and Sevim, Cigdem and Baris, Ozlem and Eser, Gizem and Yildirim, Serkan and Hacimuftuoglu, Ahmet and Buha, Aleksandra and Wallace, David R. and Tsatsakis, Aristidis and Aschner, Michael and Mezhuev, Yaroslav",
year = "2020",
abstract = "Living organisms have an innate ability to regulate the synthesis of inorganic materials, such as bones and teeth in humans. Cadmium sulfide (CdS) can be utilized as a quantum dot that functions as a unique light-emitting semiconductor nanocrystal. The increased use in CdS has led to an increased inhalation and ingestion rate of CdS by humans which requires a broader appreciation for the acute and chronic toxicity of CdS. We investigated the toxic effects of CdS on cerebellar cell cultures and rat brain. We employed a ‘green synthesis’ biosynthesis process to obtain biocompatible material that can be used in living organisms, such as Viridibacillus arenosi K64. Nanocrystal formation was initiated by adding CdCl2 (1 mM) to the cell cultures. Our in vitro results established that increased concentrations of CdS (0.1 μg/mL) lead to decreased cell viability as assessed using 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyltetrazolium bromide (MTT), total antioxidant capacity (TAC), and total oxidant status (TOS). The in vivo studies showed that exposure to CdS (1 mg/kg) glial fibrillary acidic protein (GFAP) and 8-hydroxy-2' -deoxyguanosine (8-OHdG) were increased. Collectively, we describe a model system that addresses the process from the synthesis to the neurotoxicity assessment for CdS both in vitro and in vivo. These data will be beneficial in establishing a more comprehensive pathway for the understanding of quantum dot-induced neurotoxicity.",
publisher = "Elsevier",
journal = "Toxicology Reports",
title = "Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies",
volume = "7",
pages = "637-648",
doi = "10.1016/j.toxrep.2020.04.011"
}

Varmazyari, A., Taghizadehghalehjoughi, A., Sevim, C., Baris, O., Eser, G., Yildirim, S., Hacimuftuoglu, A., Buha, A., Wallace, D. R., Tsatsakis, A., Aschner, M.,& Mezhuev, Y.. (2020). Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies. in Toxicology Reports
Elsevier., 7, 637-648.
https://doi.org/10.1016/j.toxrep.2020.04.011

Varmazyari A, Taghizadehghalehjoughi A, Sevim C, Baris O, Eser G, Yildirim S, Hacimuftuoglu A, Buha A, Wallace DR, Tsatsakis A, Aschner M, Mezhuev Y. Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies. in Toxicology Reports. 2020;7:637-648.
doi:10.1016/j.toxrep.2020.04.011 .

Varmazyari, Atefeh, Taghizadehghalehjoughi, Ali, Sevim, Cigdem, Baris, Ozlem, Eser, Gizem, Yildirim, Serkan, Hacimuftuoglu, Ahmet, Buha, Aleksandra, Wallace, David R., Tsatsakis, Aristidis, Aschner, Michael, Mezhuev, Yaroslav, "Cadmium sulfide-induced toxicity in the cortex and cerebellum: In vitro and in vivo studies" in Toxicology Reports, 7 (2020):637-648,
https://doi.org/10.1016/j.toxrep.2020.04.011 . .

TY  - JOUR
AU  - Aaseth, Jan
AU  - Buha, Aleksandra
AU  - Wallace, David R.
AU  - Bjørklund, Geir
PY  - 2020
UR  - https://farfar.pharmacy.bg.ac.rs/handle/123456789/3544
AB  - Tauopathies are a disease group characterized by either pathological accumulation or release of fragments of hyperphosphorylated tau proteins originating from the central nervous system. The tau hypotheses of Parkinson’s and Alzheimer’s diseases contain a clinically diverse spectrum of tauopathies. Studies of case records of various tauopathies may reveal clinical phenotype characteristics of the disease. In addition, improved understanding of different tauopathies would disclose environmental factors, such as xenobiotics and trace metals, that can precipitate or modify the progression of the disorder. Important for diagnostics and monitoring of these disorders is a further development of adequate biomarkers, including refined neuroimaging, or proteomics. Our goal is to provide an in-depth review of the current literature regarding the pathophysiological roles of tau proteins and the pathogenic factors leading to various tauopathies, with the perspective of future advances in potential therapeutic strategies.
PB  - MDPI
T2  - International Journal of Environmental Research and Public Health
T1  - Xenobiotics, trace metals and genetics in the pathogenesis of tauopathies
VL  - 17
IS  - 4
DO  - 10.3390/ijerph17041269
ER  - 

@article{
author = "Aaseth, Jan and Buha, Aleksandra and Wallace, David R. and Bjørklund, Geir",
year = "2020",
abstract = "Tauopathies are a disease group characterized by either pathological accumulation or release of fragments of hyperphosphorylated tau proteins originating from the central nervous system. The tau hypotheses of Parkinson’s and Alzheimer’s diseases contain a clinically diverse spectrum of tauopathies. Studies of case records of various tauopathies may reveal clinical phenotype characteristics of the disease. In addition, improved understanding of different tauopathies would disclose environmental factors, such as xenobiotics and trace metals, that can precipitate or modify the progression of the disorder. Important for diagnostics and monitoring of these disorders is a further development of adequate biomarkers, including refined neuroimaging, or proteomics. Our goal is to provide an in-depth review of the current literature regarding the pathophysiological roles of tau proteins and the pathogenic factors leading to various tauopathies, with the perspective of future advances in potential therapeutic strategies.",
publisher = "MDPI",
journal = "International Journal of Environmental Research and Public Health",
title = "Xenobiotics, trace metals and genetics in the pathogenesis of tauopathies",
volume = "17",
number = "4",
doi = "10.3390/ijerph17041269"
}

Aaseth, J., Buha, A., Wallace, D. R.,& Bjørklund, G.. (2020). Xenobiotics, trace metals and genetics in the pathogenesis of tauopathies. in International Journal of Environmental Research and Public Health
MDPI., 17(4).
https://doi.org/10.3390/ijerph17041269

Aaseth J, Buha A, Wallace DR, Bjørklund G. Xenobiotics, trace metals and genetics in the pathogenesis of tauopathies. in International Journal of Environmental Research and Public Health. 2020;17(4).
doi:10.3390/ijerph17041269 .

Aaseth, Jan, Buha, Aleksandra, Wallace, David R., Bjørklund, Geir, "Xenobiotics, trace metals and genetics in the pathogenesis of tauopathies" in International Journal of Environmental Research and Public Health, 17, no. 4 (2020),
https://doi.org/10.3390/ijerph17041269 . .