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Mitochondrial Dynamics and Peripheral NeuropathyHope Center for Neurological Disorders, Washington University, Saint Louis, Missouri, rbaloh{at}wustl.edu Peripheral neuropathy is perhaps the archetypal disease of axonal degeneration, characteristically involving degeneration of the longest axons in the body. Evidence from both inherited and acquired forms of peripheral neuropathy strongly supports that the primary pathology is in the axons themselves and points to disruption of axonal transport as an important disease mechanism. Recent studies in human genetics have further identified abnormalities in mitochondrial dynamics—the fusion, fission, and movement of mitochondria— as a player in the pathogenesis of inherited peripheral neuropathy. This review provides an update on the mechanisms of mitochondrial trafficking in axons and the emerging relationship between the disruption of mitochondrial dynamics and axonal degeneration. Evidence suggests mitochondria are a "critical cargo" whose transport is necessary for proper axonal and synaptic function. Importantly, understanding the regulation of mitochondrial movement and the consequences of decreased axonal mitochondrial function may define new paths for therapeutic agents in peripheral neuropathy and other neurodegenerative diseases. NEUROSCIENTIST 14(1):12—18, 2008. DOI: 10.1177/1073858407307354
Key Words: Mitochondria • Axon • Peripheral neuropathy • Neurodegeneration
This version was published on February
1, 2008 The Neuroscientist, Vol. 14, No. 1,
12-18 (2008) |
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