Study aim. Short telomeres forming as a result of double-stranded DNA breaks and under-replication cause arrest of the cell cycle, leading to cell senescence and death. Telomere erosion is an important mechanism regulating the aging process, limiting cell proliferation. Many studies in telomere biology in recent decades have shown that telomere DNA and telomere proteins are involved in the pathogenesis of various diseases in humans. The aim of the present work was to study telomere length in Parkinson’s disease (PD). Materials and methods. Telomere length was measured in buccal epithelial cells and leukocytes from patients with PD and a control group. Results and conclusions. Telomeres in buccal epithelial cells were found to be shorter in PD patients than in the control group; telomere lengths in blood cells were identical. It is suggested that telomere shortening in buccal epithelial cells may be due to oxidative stress and may therefore be used as a marker for PD at the early stages of disease.
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Kolyada, A.K., Vaiserman, A.M., Krasnenkov, D.S. et al. Studies of Telomere Length in Patients with Parkinson’s Disease. Neurosci Behav Physi 46, 344–347 (2016). https://doi.org/10.1007/s11055-016-0239-4
- Parkinson’s disease
- telomere theory of aging