Amyloid beta-induced glycogen synthase kinase 3β phosphorylated VDAC1 in Alzheimer's disease: Implications for synaptic dysfunction and neuronal damage

P. Hemachandra Reddy

    Research output: Contribution to journalReview article

    56 Scopus citations

    Abstract

    Glycogen synthase kinase 3 (GSK3) is a serine/threonine protein kinase that is involved in the multiple signaling processes of a cell. Increasing evidence suggests that GSK3β plays a key role in multiple cellular processes in the progression of diabetes, obesity, Alzheimer's disease (AD), Parkinson's disease (PD), inflammatory diseases, schizophrenia, bipolar and several mood disorders, and mitochondrial diseases. Recent research has found that increased GSK3β activity is linked to the pathogenesis of AD through amyloid beta (Aβ), phosphorylated tau and mitochondrial dysfunction. Recent research has also revealed that GSK3β is elevated in AD-affected tissues and is critically involved in dissociating the voltage-dependent anion channel 1 (VDAC1) protein from hexokinases, and causing disrupted glucose metabolism, mitochondrial dysfunction and activating apoptotic cell death. The purpose of this article is to review recent research that is elucidating the role of GSK3β in AD pathogenesis. We discuss the involvement of GSK3β in the phosphorylation of VDAC1 and dissociation of VADC1 with hexokinases in AD neurons.

    Original languageEnglish (US)
    Pages (from-to)1913-1921
    Number of pages9
    JournalBiochimica et Biophysica Acta - Molecular Basis of Disease
    Volume1832
    Issue number12
    DOIs
    StatePublished - Aug 28 2013

    Keywords

    • Alzheimer's disease
    • Amyloid beta
    • Amyloid beta precursor protein
    • Glycogen synthase kinase 3beta
    • Mitochondria
    • Voltage-dependent anion channel 1

    ASJC Scopus subject areas

    • Molecular Medicine
    • Molecular Biology

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