Amyloid-β and mitochondria in aging and Alzheimer's disease: Implications for synaptic damage and cognitive decline

P. Hemachandra Reddy, Maria Manczak, Peizhong Mao, Marcus J. Calkins, Arubala P. Reddy, Ulziibat Shirendeb

    Research output: Contribution to journalReview article

    159 Scopus citations

    Abstract

    This article reviews the role of amyloid-β (Aβ) and mitochondria in synaptic damage and cognitive decline found in patients with Alzheimer's disease (AD). Recent molecular, cellular, animal model, and postmortem brain studies have revealed that Aβ and mitochondrial abnormalities are key factors that cause synaptic damage and cognitive decline in AD. Aβ is reported to accumulate in subcellular compartments and to impair the normal function of neurons in AD patients. Further, recent studies using biochemical methods and electron microscopy have revealed that the accumulation of Aβ at nerve terminals affect synaptic activities, including the release of neurotransmitters and synaptic vesicles. Recent studies of the relationship between mitochondria and Aβ in AD patients suggest that in mitochondria, structural changes caused by Aβ result in increased mitochondrial fragmentation, decreased mitochondrial fusion, mitochondrial dysfunction, and synaptic damage. This paper discusses the latest research on Aβ, mitochondria, age-dependent factors of AD in the brain, and synaptic damage in AD. This paper also briefly discusses potential mitochondrial therapeutics in the treatment of patients with AD.

    Original languageEnglish (US)
    Pages (from-to)S499-S512
    JournalJournal of Alzheimer's Disease
    Volume20
    Issue numberSUPPL.2
    DOIs
    StatePublished - 2010

    Keywords

    • Amyloid-β
    • amyloid-β precursor protein
    • mitochondrial therapeutics
    • synaptic pathology

    ASJC Scopus subject areas

    • Neuroscience(all)
    • Clinical Psychology
    • Geriatrics and Gerontology
    • Psychiatry and Mental health

    Fingerprint Dive into the research topics of 'Amyloid-β and mitochondria in aging and Alzheimer's disease: Implications for synaptic damage and cognitive decline'. Together they form a unique fingerprint.

    Cite this