Research Article
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Published Online: 26 May 2009

Mitochondrial Function, Morphology, and Axonal Transport in Amyotrophic Lateral Sclerosis

Publication: Antioxidants & Redox Signaling
Volume 11, Issue Number 7

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. Antioxid. Redox Signal. 11, 1615–1626.

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cover image Antioxidants & Redox Signaling
Antioxidants & Redox Signaling
Volume 11Issue Number 7July 2009
Pages: 1615 - 1626
PubMed: 19344253

History

Published in print: July 2009
Published online: 26 May 2009
Published ahead of print: 12 May 2009
Published ahead of production: 3 April 2009
Accepted: 3 April 2009
Received: 27 March 2009

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Jordi Magrané
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York.
Giovanni Manfredi
Department of Neurology and Neuroscience, Weill Medical College of Cornell University, New York, New York.

Notes

Address reprint requests to:
Jordi Magrané
Department of Neurology and Neuroscience
Weill Medical College of Cornell University
New York, NY 10065
E-mail: [email protected]

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