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Studies of Telomere Length in Patients with Parkinson’s Disease

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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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References

  1. M. P. Longhese, “DNA damage response at functional and dysfunctional telomeres,” Genes Dev., 22, 125–140 (2008).

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  2. J. D. Griffith, L. Comeau, S. Rosenfeld, et al., “Mammalian telomeres end in a large duplex loop,” Cell, 97, 503–514 (1999).

    Article  CAS  PubMed  Google Scholar 

  3. T. de Lange, “Protection of mammalian telomeres,” Oncogene, 21, 532–540 (2002).

    Article  PubMed  Google Scholar 

  4. T. de Lange, “Shelterin: the protein complex that shapes and safeguards human telomeres,” Genes Dev., 19, 2100–2110 (2005).

    Article  PubMed  Google Scholar 

  5. C. J. Cairney and W. N. Keith, “Telomerase redefined: integrated regulation of hTR and hTERT for telomere maintenance and telomerase activity,” Biochimie, 90, 13–23 (2008).

    Article  CAS  PubMed  Google Scholar 

  6. Y. Zhao, A. J. Sfeir, Y. Zou, et al., “Telomere extension occurs at most chromosome ends and is uncoupled from fill-in in human cancer cells,” Cell, 138, 463–475 (2009).

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  7. L. Hayflick, “The limited in vitro lifetime of human diploid cell strains,” Exp. Cell Res., 37, 614–636 (1965).

    Article  CAS  PubMed  Google Scholar 

  8. J. R. Mitchell, J. Cheng, and K. Collins, “A box H/ACA small nucleolar RNA-like domain at the human telomerase RNA 3’ end,” Mol. Cell Biol., 19, 567–576 (1999).

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  9. A. Aviv, A. Valdes, J. P. Gardner, et al., “Menopause modifies the association of leukocyte telomere length with insulin resistance and inflammation,” J. Clin. Endocrinol. Metab., 91, 635–640 (2006).

    Article  CAS  PubMed  Google Scholar 

  10. T. von Zglinicki, “Oxidative stress shortens telomeres,” Trends Biochem. Sci., 27, 339–344 (2002).

    Article  Google Scholar 

  11. R. W. Frenck, Jr., E. H. Blackburn, and K. M. Shannon, “The rate of telomere sequence loss in human leukocytes varies with age,” Proc. Natl. Acad. Sci. USA, 95, 5607–5610 (1998).

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  12. U. Friedrich, E. Gries, M. Schwab, et al., “Telomere length in different tissues of elderly patients,” Mech. Ageing Dev., 119, 89–99 (2000).

    Article  CAS  PubMed  Google Scholar 

  13. H. Vaziri, W. Dragowska, R. C. Allsop, et al., “Evidence for a mitotic clock in human hematopoietic stem cells: loss of telomeric DNA with age,” Proc. Natl. Acad. Sci. USA, 91, 9857–9860 (1994).

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  14. S. Brouilette, R. K. Singh, J. R. Thompson, et al., “Cell telomere length and risk of premature myocardial infarction,” Arterioscler. Thromb. Vasc. Biol., 23, 842–846 (2003).

    Article  CAS  PubMed  Google Scholar 

  15. M. Ogami, Y. Ikura, M. Ohsawa, et al., “Telomere shortening in human coronary artery diseases,” Arterioscler. Thromb. Vasc. Biol., 24, 546–550 (2004).

    Article  CAS  PubMed  Google Scholar 

  16. O. Uziel, J. A. Singer, V. Danicek, et al., “Telomere dynamics in arteries and mononuclear cells of diabetic patients: effect of diabetes and of glycemic control,” Exp. Gerontol., 42, 971–978 (2007).

    Article  CAS  PubMed  Google Scholar 

  17. L. A. Panossian, V. R. Porter, H. F. Valenzuela, et al., “Telomere shortening in T cells correlates with Alzheimer’s disease status,” Neurobiol. Ageing, 24, 77–84 (2003).

    Article  CAS  Google Scholar 

  18. A. M. Valdes, T. Andrew, J. P. Gardner, et al., “Obesity, cigarette smoking, and telomere length in women,” Lancet, 366, 662–664 (2005).

    Article  CAS  PubMed  Google Scholar 

  19. E. S. Epel, E. H. Blackburn, F. Lin, et al., “Accelerated telomere shortening in response to life stress,” Proc. Natl. Acad. Sci. USA, 101, 17312–17315 (2004).

    Article  PubMed Central  CAS  PubMed  Google Scholar 

  20. R. M. Cawthon, “Telomere length measurement by a novel monochrome multiplex quantitative PCR method,” Nucl. Acids Res., 37, 21 (2009).

    Article  Google Scholar 

  21. R. M. Cawthon, “Telomere measurement by quantitative PCR,” Nucl. Acids Res., 30, 47 (2002).

    Article  Google Scholar 

  22. J. Z. Guan, T. Maeda, M. Sugano, et al., “A percentage analysis of the telomere length in Parkinson’s disease patients,” J. Gerontol. A. Biol. Sci. Med. Sci., 63, 467–473 (2008).

    Article  PubMed  Google Scholar 

  23. H. Wang, H. Chen, X. Gao, et al., “Telomere length and risk of Parkinson’s disease,” Mov. Disord., 23, 302–305 (2008).

    Article  PubMed Central  PubMed  Google Scholar 

  24. T. Maeda, J. Z. Guan, J. Oyama, et al., “Aging-associated alteration of subtelomeric methylation in Parkinson’s disease,” J. Gerontol. A. Biol. Sci. Med. Sci., 64, 949–955 (2009).

    Article  PubMed  Google Scholar 

  25. P. Thomas, N. J. O’Callaghan, and M. Fenech, “Telomere length in white blood cells, buccal cells and brain tissue and its variation with ageing and Alzheimer’s disease,” Mech. Ageing Dev., 129, 183–190 (2008).

    Article  CAS  PubMed  Google Scholar 

  26. C. Cipriano, S. Tesei, M. Malavolta, et al., “Accumulation of cells with short telomeres is associated with impaired zinc homeostasis and inflammation in old hypertensive participants,” J. Gerontol. A. Biol. Sci. Med. Sci., 64, 745–751 (2009).

    Article  PubMed  Google Scholar 

  27. P. Ilmonen, A. Kotrschal, and D. J. Penn, “Telomere attrition due to infection,” PLoS One, 3, 2143 (2008).

    Article  Google Scholar 

  28. J. J. Carreo, P. Stenvinkel, B. Fellstrom, et al., “Telomere attrition is associated with inflammation, low fetuin-A levels and high mortality in prevalent haemodialysis patients,” J. Int. Med., 263, 302–312 (2008).

    Article  Google Scholar 

  29. A. Aviv, “Telomeres and human aging: facts and fi bs,” Sci. Aging Knowl. Environ., 51, 43 (2004).

    Google Scholar 

  30. S. Kawanishi and O. Oikawa, “Mechanism of telomere shortening by oxidative stress,” Ann. NY Acad. Sci., 1019, 278–284 (2004).

    Article  CAS  PubMed  Google Scholar 

  31. N. Sitte, G. Saretzki, and T. von Zglinicki, “Accelerated telomere shortening in fibroblasts after extended periods of confluency,” Free Radic. Biol. Med., 24, 885–893 (1998).

    Article  CAS  PubMed  Google Scholar 

  32. T. von Zglinicki, C. Martin-Ruiz, and G. Saretzki, “Telomeres, cell senescence and human ageing,” Signal Transduct., 3, 103–114 (2005).

    Article  Google Scholar 

  33. S. Petersen, G. Saretzki, and T. von Zglinicki, “Preferential accumulation of single-stranded regions in telomeres of human fibroblasts,” Exp. Cell Res., 239, 152–160 (1998).

    Article  CAS  PubMed  Google Scholar 

  34. T. Richter, G. Saretzki, G. Nelson, et al., “TRF2 overexpression diminishes repair of telomeric single-strand breaks and accelerates telomere shortening in human fibroblasts,” Mech. Ageing Dev., 128, 340–345 (2007).

    Article  CAS  PubMed  Google Scholar 

  35. O. Beyne-Rauzy, C. Recher, N. Sastugue, et al., “Tumor necrosis factor alpha induces senescence and chromosomal instability in human leukemic cells,” Oncogene, 23, 7507–7516 (2004).

    Article  CAS  PubMed  Google Scholar 

  36. A. A. Boldyrev, “Oxidative stress and the brain,” Soros. Obraz. Zh., No. 4, 21–28 (2001).

  37. K. M. Dyumaev, T. A. Voronina, and L. D. Smirnov, Antioxidants in the Prophylaxis and Treatment of CNS Pathology, Institute of Biomedical Chemistry Press, Russian Academy of Medical Sciences, Moscow (1995).

    Google Scholar 

  38. I. A. Zavalishina, N. N. Yakhno, and S. I. Gavrilova, Neurodege nerative Diseases and Aging, A.A.A., Moscow (2001).

    Google Scholar 

  39. K. Koziorowski and J. Jasztal, “Factors which can play important role in pathogenesis of Parkinson disease,” Neurol. Neurochir. Pol., 33, 907–921 (1999).

    CAS  PubMed  Google Scholar 

  40. D. J. Moore, V. L. Dawson, and T. M. Sawson, “Molecular pathophysiology of Parkinson’s disease,” Annu. Rev. Neurosci., 28, 57–87 (2005).

    Article  CAS  PubMed  Google Scholar 

  41. B. Thomas and M. F. Beal, “Parkinson’s disease,” Hum. Mol. Genet., 16, 183–194 (2007).

    Article  Google Scholar 

  42. J. R. Vaughan, M. J. Farrer, Z. K. Wszolek, et al., “Sequencing of the alphasynuclein gene in a large series of cases of familial Parkinson’s disease fails to reveal any further mutations,” Hum. Mol. Genet., 7, 751–753 (1998).

    Article  CAS  PubMed  Google Scholar 

  43. M. W. Fariss, C. B. Chan, M. Patel, et al., “Role of mitochondria in toxic oxidative stress,” Mol. Interv., 5, 94–111 (2005).

    Article  CAS  PubMed  Google Scholar 

  44. M. Naoi and W. Maruyama, “Cell death of dopamine neurons in aging and Parkinson’s disease,” Mech. Ageing Dev., 111, 175–188 (1999).

    Article  CAS  PubMed  Google Scholar 

  45. N. Ogawa and A. Mori, “Parkinson’s disease, dopamine and free radicals,” in: Oxidative Stress and Aging, R. G. Cutler (ed.), New York (1995), pp. 303–309.

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Authors and Affiliations

  1. Chebotarev Institute of Gerontology, Ukrainian National Academy of Medical Sciences, Kiev, Ukraine

    A. K. Kolyada, A. M. Vaiserman, D. S. Krasnenkov & I. N. Karaban’

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  1. A. K. Kolyada
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  2. A. M. Vaiserman
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  3. D. S. Krasnenkov
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  4. I. N. Karaban’
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Correspondence to A. K. Kolyada.

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Translated from Zhurnal Nevrologii i Psikhiatrii imeni S. S. Korsakova, Vol. 114, No. 8, Iss. I, pp. 58–61, August, 2014.

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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

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