NeuroMolecular Medicine

, Volume 15, Issue 1, pp 25–48 | Cite as

Telomere Shortening and Alzheimer’s Disease

  • Zhiyou CaiEmail author
  • Liang-Jun Yan
  • Anna Ratka
Review Paper


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.


Telomere Telomere shortening Alzheimer’s disease 





Alzheimer’s disease


Amyloid precursor protein


Beta-site APP-cleaving enzyme


Blood brain barrier


Breakage/fusion/bridge cycle


Cerebral autosomal dominant arteriopathy and leukoencephalopathy


Chronic obstructive pulmonary disease


Cyclooxygenase 2


C-reactive protein


Cardiovascular disease


Endothelial nitric oxide synthase


Inter-cellular adhesion molecule 1


Extracellular matrix


Granulocyte–macrophage colony-stimulating factor


Huntington’s disease




Leukemia inhibitory factor




Interleukin-1 receptor-associated kinase


Iron-responsive element


Low-density lipoprotein receptor-related protein 1


Mitogen-activated protein kinase


Mild cognitive impairment


Macrophage chemoattractant protein 1


Myelodysplastic syndromes


Matrix metalloproteinases


Mini Mental Status Examination


Nuclear factor-kappa B


Neurofibrillary tangles


Nitric oxide


Obstructive sleep apnea


Parkinson’s disease


Receptor for advanced glycation end products


Reactive oxygen species


Sleep apnea syndrome


Transforming growth factor beta


Tumor necrosis factor-alpha


Tumor necrosis factor receptor


TNF receptor-associated death domain





This work was supported by the National Nature Science Foundation of China Grant (81070878/H0902) to Prof. Bin Zhao.


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Copyright information

© Springer Science+Business Media New York 2012

Authors and Affiliations

  1. 1.Department of Neurology, Lu’an People’s HospitalThe Lu’an Affiliated Hospital of Anhui Medical UniversityDistrict of Jin’an, Lu’anChina
  2. 2.West Anhui Health Vocational CollegeLu’anChina
  3. 3.Department of Pharmaceutical SciencesTexas A&M Health Science CenterKingsvilleUSA
  4. 4.Department of Pharmacology & NeuroscienceUniversity of North Texas Health Science CenterFort WorthUSA

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