Mitochondrial accumulation of APP and Abeta: significance for Alzheimer disease pathogenesis

Pavel F Pavlov, Anna Camilla Hansson Petersen, Elzbieta Glaser, Maria Ankarcrona

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

    67 Citationer (Scopus)

    Abstract

    Accumulating evidence suggest that alterations in energy metabolism are among the earliest events that occur in the Alzheimer disease (AD) affected brain. Energy consumption is drastically decreased in the AD-affected regions of cerebral cortex and hippocampus pointing towards compromised mitochondrial function of neurons within specific brain regions. This is accompanied by an elevated production of reactive oxygen species contributing to increased rates of neuronal loss in the AD-affected brain regions. In this review, we will discuss the role of mitochondrial function and dysfunction in AD. We will focus on the consequences of amyloid precursor protein and amyloid-beta peptide accumulation in mitochondria and their involvement in AD pathogenesis.
    OriginalsprogEngelsk
    TidsskriftJournal of Cellular and Molecular Medicine
    Vol/bind13
    Udgave nummer10
    Sider (fra-til)4137-45
    Antal sider9
    ISSN1582-1838
    DOI
    StatusUdgivet - 2009

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