Mitochondria-targeted antioxidant SS31 prevents Amyloid beta-induced mitochondrial abnormalities and synaptic degeneration in Alzheimer's disease

Marcus J. Calkins, Maria Manczak, P (Hemachandra) Reddy

    Research output: Contribution to journalArticle

    34 Scopus citations


    In neuronal systems, the health and activity of mitochondria and synapses are tightly coupled. For this reason, it has been postulated that mitochondrial abnormalities may, at least in part, drive neurodegeneration in conditions such as Alzheimer's disease (AD). Mounting evidence from multiple Alzheimer's disease cell and mouse models and postmortem brains suggest that loss of mitochondrial integrity may be a key factor that mediates synaptic loss. Therefore, the prevention or rescue of mitochondrial dysfunction may help delay or altogether prevent AD-associated neurodegeneration. Since mitochondrial health is heavily dependent on antioxidant defenses, researchers have begun to explore the use of mitochondria-targeted antioxidants as therapeutic tools to prevent neurodegenerative diseases. This review will highlight advances made using a model mitochondria-targeted antioxidant peptide, SS31, as a potential treatment for AD.

    Original languageEnglish (US)
    Pages (from-to)1103-1119
    Number of pages17
    Issue number10
    Publication statusPublished - Oct 16 2012



    • Alzheimer's
    • Antioxidant
    • Mitochondria
    • SS31

    ASJC Scopus subject areas

    • Molecular Medicine
    • Pharmaceutical Science

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