Mitochondrial fragmentation in neurodegeneration

    Authors

    A. B. Knott; G. Perkins; R. Schwarzenbacher;E. Bossy-Wetzel

    Comments

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    Abbreviated Journal Title

    Nat. Rev. Neurosci.

    Keywords

    DIFFERENTIATION-ASSOCIATED PROTEIN-1; DYNAMIN-RELATED GTPASE; HUMAN; SKELETAL-MUSCLE; MARIE-TOOTH-DISEASE; CYCLIN-DEPENDENT KINASES; CELL-DEATH; ALZHEIMERS-DISEASE; OPTIC ATROPHY; OXIDATIVE DAMAGE; DNA; MUTATIONS; Neurosciences

    Abstract

    Mitochondria are remarkably dynamic organelles that migrate, divide and fuse. Cycles of mitochondrial fission and fusion ensure metabolite and mitochondrial DNA mixing and dictate organelle shape, number and bioenergetic functionality. There is mounting evidence that mitochondrial dysfunction is an early and causal event in neurodegeneration. Mutations in the mitochondrial fusion GTPases mitofusin 2 and optic atrophy 1, neurotoxins and oxidative stress all disrupt the cable-like morphology of functional mitochondria. This results in impaired bioenergetics and mitochondrial migration, and can trigger neurodegeneration. These findings suggest potential new treatment avenues for neurodegenerative diseases.

    Journal Title

    Nature Reviews Neuroscience

    Volume

    9

    Issue/Number

    7

    Publication Date

    1-1-2008

    Document Type

    Review

    Language

    English

    First Page

    505

    Last Page

    518

    WOS Identifier

    WOS:000256929300011

    ISSN

    1471-003X

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