Aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction in Alzheimer's disease: Implications for early intervention and therapeutics

Peizhong Mao, P. Hemachandra Reddy

Research output: Contribution to journalReview articlepeer-review

189 Scopus citations

Abstract

Alzheimer's disease (AD) is an age-related progressive neurodegenerative disease affecting thousands of people in the world and effective treatment is still not available. Over two decades of intense research using AD postmortem brains, transgenic mouse and cell models of amyloid precursor protein and tau revealed that amyloid beta (Aβ) and hyperphosphorylated tau are synergistically involved in triggering disease progression. Accumulating evidence also revealed that aging and amyloid beta-induced oxidative DNA damage and mitochondrial dysfunction initiate and contributes to the development and progression of the disease. The purpose of this article is to summarize the latest progress in aging and AD, with a special emphasis on the mitochondria, oxidative DNA damage including methods of its measurement. It also discusses the therapeutic approaches against oxidative DNA damage and treatment strategies in AD.

Original languageEnglish (US)
Pages (from-to)1359-1370
Number of pages12
JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
Volume1812
Issue number11
DOIs
StatePublished - Nov 2011
Externally publishedYes

Keywords

  • Amyloid-β
  • Antioxidant
  • DNA repair
  • Oxidative stress
  • P53
  • Telomere

ASJC Scopus subject areas

  • Molecular Medicine
  • Molecular Biology

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