NeuroMolecular Medicine

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

Telomere Shortening and Alzheimer’s Disease

Review Paper

Abstract

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.

Keywords

Telomere Telomere shortening Alzheimer’s disease 

Abbreviations

Aβ

Beta-amyloid

AD

Alzheimer’s disease

APP

Amyloid precursor protein

BACE

Beta-site APP-cleaving enzyme

BBB

Blood brain barrier

BFB

Breakage/fusion/bridge cycle

CADASIL

Cerebral autosomal dominant arteriopathy and leukoencephalopathy

COPD

Chronic obstructive pulmonary disease

Cox-2

Cyclooxygenase 2

CRP

C-reactive protein

CVD

Cardiovascular disease

eNOS

Endothelial nitric oxide synthase

ICAM-1

Inter-cellular adhesion molecule 1

ECM

Extracellular matrix

GM-CSF

Granulocyte–macrophage colony-stimulating factor

HD

Huntington’s disease

IFN

Interferon

LIF

Leukemia inhibitory factor

IL

Interleukin

IRAK

Interleukin-1 receptor-associated kinase

IRE

Iron-responsive element

LRP-1

Low-density lipoprotein receptor-related protein 1

MAPK

Mitogen-activated protein kinase

MCI

Mild cognitive impairment

MCP-1

Macrophage chemoattractant protein 1

MDS

Myelodysplastic syndromes

MMPs

Matrix metalloproteinases

MMSE

Mini Mental Status Examination

NF-κB

Nuclear factor-kappa B

NFT

Neurofibrillary tangles

NO

Nitric oxide

OSA

Obstructive sleep apnea

PD

Parkinson’s disease

RAGE

Receptor for advanced glycation end products

ROS

Reactive oxygen species

SAS

Sleep apnea syndrome

TGF-β

Transforming growth factor beta

TNF-α

Tumor necrosis factor-alpha

TNFR

Tumor necrosis factor receptor

TRADD

TNF receptor-associated death domain

8-oxodG

8-Oxo-2′-deoxyguanosine

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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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