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 journalArticle

    143 Citations (Scopus)

    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

    Fingerprint

    Amyloid
    DNA Damage
    Alzheimer Disease
    Disease Progression
    Amyloid beta-Protein Precursor
    Therapeutics
    Neurodegenerative Diseases
    Transgenic Mice
    Mitochondria
    Brain
    Research

    Keywords

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

    ASJC Scopus subject areas

    • Molecular Biology
    • Molecular Medicine

    Cite this

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