Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease

P. Hemachandra Reddy, M. Flint Beal

    Research output: Contribution to journalArticle

    536 Scopus citations

    Abstract

    Recent studies of postmortem brains from Alzheimer's disease (AD) patients and transgenic mouse models of AD suggest that oxidative damage, induced by amyloid β (Aβ), is associated with mitochondria early in AD progression. Aβ and amyloid-precursor protein are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron-transport chain, increase reactive oxygen species production, cause mitochondrial damage and prevent neurons from functioning normally. Furthermore, accumulation of Aβ at synaptic terminals might contribute to synaptic damage and cognitive decline in patients with AD. Here, we describe recent studies regarding the roles of Aβ and mitochondrial function in AD progression and particularly in synaptic damage and cognitive decline.

    Original languageEnglish (US)
    Pages (from-to)45-53
    Number of pages9
    JournalTrends in Molecular Medicine
    Volume14
    Issue number2
    DOIs
    StatePublished - Feb 2008

    ASJC Scopus subject areas

    • Molecular Medicine
    • Molecular Biology

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