Premature centromere division, or premature centromere separation (PCS), occurs when chromatid separation is dysfunctional, occurring earlier than usual during the interphase stage of mitosis. This phenomenon, seen in Robert's syndrome and various cancers, has also been documented in peripheral as well as neuronal cells of Alzheimer's disease (AD). In the latter instances, fluorescent in situ hybridization (FISH), applied to the centromere region of the X-chromosome in interphase nuclei of lymphocytes from peripheral blood in AD patients, demonstrated premature chromosomal separation before mitotic metaphase directly after completion of DNA replication in G(2) phase of the cell cycle. Furthermore, and perhaps unexpectedly given the presumptive post-mitotic status of terminally differentiated neurons, neurons in AD patients also showed significantly increased levels of PCS of the X-chromosome. Taken together with other phenomena such as cell cycle re-activation and ectopic re-expression... of cyclins and cyclin dependent proteins, we propose that AD is an oncogenic phenotype leading to accelarated aging of the affected brain.
TY - JOUR
AU - Bajić, Vladan
AU - Potparević, Biljana
AU - Živković, Lada
AU - Bonda, David J.
AU - Siedlak, Sandra L.
AU - Casadesus, Gemma
AU - Lee, Hyoung-Gon
AU - Smith, Mark A.
PY - 2009
UR - https://farfar.pharmacy.bg.ac.rs/handle/123456789/1212
AB - Premature centromere division, or premature centromere separation (PCS), occurs when chromatid separation is dysfunctional, occurring earlier than usual during the interphase stage of mitosis. This phenomenon, seen in Robert's syndrome and various cancers, has also been documented in peripheral as well as neuronal cells of Alzheimer's disease (AD). In the latter instances, fluorescent in situ hybridization (FISH), applied to the centromere region of the X-chromosome in interphase nuclei of lymphocytes from peripheral blood in AD patients, demonstrated premature chromosomal separation before mitotic metaphase directly after completion of DNA replication in G(2) phase of the cell cycle. Furthermore, and perhaps unexpectedly given the presumptive post-mitotic status of terminally differentiated neurons, neurons in AD patients also showed significantly increased levels of PCS of the X-chromosome. Taken together with other phenomena such as cell cycle re-activation and ectopic re-expression of cyclins and cyclin dependent proteins, we propose that AD is an oncogenic phenotype leading to accelarated aging of the affected brain.
PB - Churchill Livingstone, Edinburgh
T2 - Medical Hypotheses
T1 - The X-chromosome instability phenotype in Alzheimer's disease: A clinical sign of accelerating aging?
VL - 73
IS - 6
SP - 917
EP - 920
DO - 10.1016/j.mehy.2009.06.046
UR - conv_2258
ER -
@article{
author = "Bajić, Vladan and Potparević, Biljana and Živković, Lada and Bonda, David J. and Siedlak, Sandra L. and Casadesus, Gemma and Lee, Hyoung-Gon and Smith, Mark A.",
year = "2009",
abstract = "Premature centromere division, or premature centromere separation (PCS), occurs when chromatid separation is dysfunctional, occurring earlier than usual during the interphase stage of mitosis. This phenomenon, seen in Robert's syndrome and various cancers, has also been documented in peripheral as well as neuronal cells of Alzheimer's disease (AD). In the latter instances, fluorescent in situ hybridization (FISH), applied to the centromere region of the X-chromosome in interphase nuclei of lymphocytes from peripheral blood in AD patients, demonstrated premature chromosomal separation before mitotic metaphase directly after completion of DNA replication in G(2) phase of the cell cycle. Furthermore, and perhaps unexpectedly given the presumptive post-mitotic status of terminally differentiated neurons, neurons in AD patients also showed significantly increased levels of PCS of the X-chromosome. Taken together with other phenomena such as cell cycle re-activation and ectopic re-expression of cyclins and cyclin dependent proteins, we propose that AD is an oncogenic phenotype leading to accelarated aging of the affected brain.",
publisher = "Churchill Livingstone, Edinburgh",
journal = "Medical Hypotheses",
title = "The X-chromosome instability phenotype in Alzheimer's disease: A clinical sign of accelerating aging?",
volume = "73",
number = "6",
pages = "917-920",
doi = "10.1016/j.mehy.2009.06.046",
url = "conv_2258"
}
Bajić, V., Potparević, B., Živković, L., Bonda, D. J., Siedlak, S. L., Casadesus, G., Lee, H.,& Smith, M. A.. (2009). The X-chromosome instability phenotype in Alzheimer's disease: A clinical sign of accelerating aging?. in Medical Hypotheses
Churchill Livingstone, Edinburgh., 73(6), 917-920.
https://doi.org/10.1016/j.mehy.2009.06.046
conv_2258
Bajić V, Potparević B, Živković L, Bonda DJ, Siedlak SL, Casadesus G, Lee H, Smith MA. The X-chromosome instability phenotype in Alzheimer's disease: A clinical sign of accelerating aging?. in Medical Hypotheses. 2009;73(6):917-920.
doi:10.1016/j.mehy.2009.06.046
conv_2258 .
Bajić, Vladan, Potparević, Biljana, Živković, Lada, Bonda, David J., Siedlak, Sandra L., Casadesus, Gemma, Lee, Hyoung-Gon, Smith, Mark A., "The X-chromosome instability phenotype in Alzheimer's disease: A clinical sign of accelerating aging?" in Medical Hypotheses, 73, no. 6 (2009):917-920,
https://doi.org/10.1016/j.mehy.2009.06.046 .,
conv_2258 .
