Are mitochondria critical in the pathogenesis of Alzheimer's disease?

P. Hemachandra Reddy, M. Flint Beal

    Research output: Contribution to journalReview articlepeer-review

    232 Scopus citations


    This review summarizes recent findings that suggest a causal connection between mitochondrial abnormalities and sporadic Alzheimer's disease (AD). Genetic causes of AD are known only for a small proportion of familial AD patients, but for a majority of sporadic AD patients, genetic causal factors are still unknown. Currently, there are no early detectable biomarkers for sporadic AD, and there is a lack of understanding of the pathophysiology of the disease. Findings from recent genetic studies of AD pathogenesis suggest that mitochondrial defects may play an important role in sporadic AD progression, and that mitochondrial abnormalities and oxidative damage may play a significant role in the progression of familial AD. Findings from biochemical studies, in vitro studies, gene expression studies, and animal model studies of AD are reviewed, and the possible contribution of mitochondrial mutations to late-onset sporadic AD is discussed.

    Original languageEnglish (US)
    Pages (from-to)618-632
    Number of pages15
    JournalBrain Research Reviews
    Issue number3
    StatePublished - Nov 2005


    • In vitro studies
    • Mitochondria
    • Mitochondrial gene expression
    • Mitochondrial mutations
    • Oxidative damage
    • Peripheral cells
    • Sporadic Alzheimer's disease
    • Transgenic mice

    ASJC Scopus subject areas

    • Neuroscience(all)
    • Clinical Neurology

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