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Antioxid Redox Signal. 2009 Jul;11(7):1615-26. doi: 10.1089/ARS.2009.2604.

Mitochondrial function, morphology, and axonal transport in amyotrophic lateral sclerosis.

Author information

1
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York 10065, USA. jom2025@med.cornell.edu

Abstract

Perturbation of organellar axonal transport is increasingly recognized as an important contributor in a number of neurodegenerative diseases. Although the specificity of this impairment remains to be elucidated, growing evidence suggests that in certain disease conditions, mitochondria are affected primarily by transport defects. Many hypotheses have been formulated to explain the pathogenic mechanisms involved in amyotrophic lateral sclerosis (ALS). The mutations described so far in genetic forms of ALS (familial ALS, fALS) affect proteins involved in a wide variety of cellular mechanisms, including free radical scavenging, energy metabolism, axonal transport, RNA processing, DNA repair, vesicular transport, and angiogenesis. Here we review the current knowledge on mitochondrial transport and its role in ALS.

PMID:
19344253
PMCID:
PMC2789440
DOI:
10.1089/ARS.2009.2604
[Indexed for MEDLINE]
Free PMC Article

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