TY  - JOUR
AU  - Živković, Lada
AU  - Spremo-Potparević, Biljana
AU  - Siedlak, Sandra L.
AU  - Perry, George
AU  - Plećaš-Solarović, Bosiljka
AU  - Milicević, Zorana
AU  - Bajić, Vladan P.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5681
AB  - While Alzheimer disease (AD) is considered a neurodegenerative disorder, the importance of chromosome instability in non-neuronal cells is equally important, not only for shedding light on the etiology of the disease, but also for possible diagnostic purposes and monitoring the progress of the disease. Here, we evaluated the frequency of DNA damage and expression of premature centromere division (PCD) in peripheral blood lymphocytes of sporadic AD patients, age-matched and young controls. The results show that in male patients with AD, the frequencies of PCD and DNA damage were significantly greater (88%, p LT 0.01 and 38%, p LT 0.05, respectively) than in age-matched control group. AD females had significantly increased frequency of PCD (134%, p LT 0.01) as well as a higher frequency of DNA damage (37%, p LT 0.05). Ageing per se, both in males and females, shows significant increase of percentages of PCD (2.3 times, p LT 0.01 and 2.8 times, p LT 0.01, respectively) and DNA damage (63%, p LT 0.01 and 50%, p LT 0.01, respectively) comparing with young controls. In addition, a strong (R-2 = 0.873, n = 6) and significant (p LT 0.01) correlation between the frequencies of PCD and DNA damage was found in all examined groups. We may conclude that the increases in both parameters evaluated in this study are not only associated with normal ageing processes, but are markedly and significantly intensified in AD pathogenesis. Thus, our data support the view that AD is a generalized systemic disease, at least as for the increased DNA damage and PCD incidence in peripheral blood cells. copyright (C) 2013 S. Karger AG, Basel
T2  - Neurodegenerative diseases
T1  - DNA Damage in Alzheimer Disease Lymphocytes and Its Relation to Premature Centromere Division
VL  - 12
IS  - 3
SP  - 156
EP  - 163
DO  - 10.1159/000346114
ER  - 

@article{
author = "Živković, Lada and Spremo-Potparević, Biljana and Siedlak, Sandra L. and Perry, George and Plećaš-Solarović, Bosiljka and Milicević, Zorana and Bajić, Vladan P.",
year = "2013",
abstract = "While Alzheimer disease (AD) is considered a neurodegenerative disorder, the importance of chromosome instability in non-neuronal cells is equally important, not only for shedding light on the etiology of the disease, but also for possible diagnostic purposes and monitoring the progress of the disease. Here, we evaluated the frequency of DNA damage and expression of premature centromere division (PCD) in peripheral blood lymphocytes of sporadic AD patients, age-matched and young controls. The results show that in male patients with AD, the frequencies of PCD and DNA damage were significantly greater (88%, p LT 0.01 and 38%, p LT 0.05, respectively) than in age-matched control group. AD females had significantly increased frequency of PCD (134%, p LT 0.01) as well as a higher frequency of DNA damage (37%, p LT 0.05). Ageing per se, both in males and females, shows significant increase of percentages of PCD (2.3 times, p LT 0.01 and 2.8 times, p LT 0.01, respectively) and DNA damage (63%, p LT 0.01 and 50%, p LT 0.01, respectively) comparing with young controls. In addition, a strong (R-2 = 0.873, n = 6) and significant (p LT 0.01) correlation between the frequencies of PCD and DNA damage was found in all examined groups. We may conclude that the increases in both parameters evaluated in this study are not only associated with normal ageing processes, but are markedly and significantly intensified in AD pathogenesis. Thus, our data support the view that AD is a generalized systemic disease, at least as for the increased DNA damage and PCD incidence in peripheral blood cells. copyright (C) 2013 S. Karger AG, Basel",
journal = "Neurodegenerative diseases",
title = "DNA Damage in Alzheimer Disease Lymphocytes and Its Relation to Premature Centromere Division",
volume = "12",
number = "3",
pages = "156-163",
doi = "10.1159/000346114"
}

Živković, L., Spremo-Potparević, B., Siedlak, S. L., Perry, G., Plećaš-Solarović, B., Milicević, Z.,& Bajić, V. P.. (2013). DNA Damage in Alzheimer Disease Lymphocytes and Its Relation to Premature Centromere Division. in Neurodegenerative diseases, 12(3), 156-163.
https://doi.org/10.1159/000346114

Živković L, Spremo-Potparević B, Siedlak SL, Perry G, Plećaš-Solarović B, Milicević Z, Bajić VP. DNA Damage in Alzheimer Disease Lymphocytes and Its Relation to Premature Centromere Division. in Neurodegenerative diseases. 2013;12(3):156-163.
doi:10.1159/000346114 .

Živković, Lada, Spremo-Potparević, Biljana, Siedlak, Sandra L., Perry, George, Plećaš-Solarović, Bosiljka, Milicević, Zorana, Bajić, Vladan P., "DNA Damage in Alzheimer Disease Lymphocytes and Its Relation to Premature Centromere Division" in Neurodegenerative diseases, 12, no. 3 (2013):156-163,
https://doi.org/10.1159/000346114 . .

TY  - JOUR
AU  - Bajić, Vladan P.
AU  - Su, Bo
AU  - Lee, Hyoung-Gon
AU  - Kudo, Wataru
AU  - Siedlak, Sandra L.
AU  - Živković, Lada
AU  - Spremo-Potparević, Biljana
AU  - Đelić, Ninoslav
AU  - Milicević, Zorana
AU  - Singh, Avneet K.
AU  - Fahmy, Lara M.
AU  - Wang, Xinglong
AU  - Smith, Mark A.
AU  - Zhu, Xiongwei
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4429
AB  - Post-mitotic neurons are typically terminally differentiated and in a quiescent status. However, in Alzheimer disease (AD), many neurons display ectopic re-expression of cell cycle-related proteins. Cyclin-dependent kinase 11 (CDK11) mRNA produces a 110-kDa protein (CDK11(p110)) throughout the cell cycle, a 58-kDa protein (CDK11(p58)) that is specifically translated from an internal ribosome entry site and expressed only in the G(2)/M phase of the cell cycle, and a 46-kDa protein (CDK11(p46)) that is considered to be apoptosis specific. CDK11 is required for sister chromatid cohesion and the completion of mitosis. In this study, we found that the expression patterns of CDK11 vary such that cytoplasmic CDK11 is increased in AD cellular processes, compared to a pronounced nuclear expression pattern in most controls. We also investigated the effect of amyloid precursor protein (APP) on CDK11 expression in vitro by using M17 cells overexpressing wild-type APP and APP Swedish mutant phenotype and found increased CDK11 expression compared to empty vector. In addition, amyloid-beta(25-35) resulted in increased CDK11 in M17 cells. These data suggest that CDK11 may play a vital role in cell cycle re-entry in AD neurons in an APP-dependent manner, thus presenting an intriguing novel function of the APP signaling pathway in AD.
T2  - Cellular and Molecular Biology Letters
T1  - Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease
VL  - 16
IS  - 3
SP  - 359
EP  - 372
DO  - 10.2478/s11658-011-0011-2
ER  - 

@article{
author = "Bajić, Vladan P. and Su, Bo and Lee, Hyoung-Gon and Kudo, Wataru and Siedlak, Sandra L. and Živković, Lada and Spremo-Potparević, Biljana and Đelić, Ninoslav and Milicević, Zorana and Singh, Avneet K. and Fahmy, Lara M. and Wang, Xinglong and Smith, Mark A. and Zhu, Xiongwei",
year = "2011",
abstract = "Post-mitotic neurons are typically terminally differentiated and in a quiescent status. However, in Alzheimer disease (AD), many neurons display ectopic re-expression of cell cycle-related proteins. Cyclin-dependent kinase 11 (CDK11) mRNA produces a 110-kDa protein (CDK11(p110)) throughout the cell cycle, a 58-kDa protein (CDK11(p58)) that is specifically translated from an internal ribosome entry site and expressed only in the G(2)/M phase of the cell cycle, and a 46-kDa protein (CDK11(p46)) that is considered to be apoptosis specific. CDK11 is required for sister chromatid cohesion and the completion of mitosis. In this study, we found that the expression patterns of CDK11 vary such that cytoplasmic CDK11 is increased in AD cellular processes, compared to a pronounced nuclear expression pattern in most controls. We also investigated the effect of amyloid precursor protein (APP) on CDK11 expression in vitro by using M17 cells overexpressing wild-type APP and APP Swedish mutant phenotype and found increased CDK11 expression compared to empty vector. In addition, amyloid-beta(25-35) resulted in increased CDK11 in M17 cells. These data suggest that CDK11 may play a vital role in cell cycle re-entry in AD neurons in an APP-dependent manner, thus presenting an intriguing novel function of the APP signaling pathway in AD.",
journal = "Cellular and Molecular Biology Letters",
title = "Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease",
volume = "16",
number = "3",
pages = "359-372",
doi = "10.2478/s11658-011-0011-2"
}

Bajić, V. P., Su, B., Lee, H., Kudo, W., Siedlak, S. L., Živković, L., Spremo-Potparević, B., Đelić, N., Milicević, Z., Singh, A. K., Fahmy, L. M., Wang, X., Smith, M. A.,& Zhu, X.. (2011). Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease. in Cellular and Molecular Biology Letters, 16(3), 359-372.
https://doi.org/10.2478/s11658-011-0011-2

Bajić VP, Su B, Lee H, Kudo W, Siedlak SL, Živković L, Spremo-Potparević B, Đelić N, Milicević Z, Singh AK, Fahmy LM, Wang X, Smith MA, Zhu X. Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease. in Cellular and Molecular Biology Letters. 2011;16(3):359-372.
doi:10.2478/s11658-011-0011-2 .

Bajić, Vladan P., Su, Bo, Lee, Hyoung-Gon, Kudo, Wataru, Siedlak, Sandra L., Živković, Lada, Spremo-Potparević, Biljana, Đelić, Ninoslav, Milicević, Zorana, Singh, Avneet K., Fahmy, Lara M., Wang, Xinglong, Smith, Mark A., Zhu, Xiongwei, "Mislocalization of CDK11/PITSLRE, a regulator of the G2/M phase of the cell cycle, in Alzheimer disease" in Cellular and Molecular Biology Letters, 16, no. 3 (2011):359-372,
https://doi.org/10.2478/s11658-011-0011-2 . .