Author: Cai Z, Yan LJ, Ratka A.
Department of Neurology, Lu'an People's Hospital, The Lu'an Affiliated Hospital of Anhui Medical University, 27 Wanxi Western Road, District of Jin'an, Lu'an, 237005, Anhui Province, China, firstname.lastname@example.org.
Conference/Journal: Neuromolecular Med.
Date published: 2012 Nov 16
Other: Word Count: 116
Telomeres, at the ends of chromosomes and strands of genetic material, become shorter as cells divide in the process of aging. Telomere length has been considered as a biological marker of age. Telomere length shortening has also been evidenced as the causable role in age-related neurodegenerative diseases, including Alzheimer's disease (AD). It has been demonstrated that telomere shortening has been associated with cognitive impairment, amyloid pathology and hyper-phosphorylation of tau in AD and plays an important role in the pathogenesis of AD via the mechanism of oxidative stress and inflammation. However, it seems that there is no relationship between telomere shortening and AD. Therefore, it is essential for further clarification of telomere-related pathogenesis in AD.