Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/106788
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Type: Journal article
Title: Mitochondrial dysfunction in amyotrophic lateral sclerosis - a valid pharmacological target?
Author: Muyderman, H.
Chen, T.
Citation: British Journal of Pharmacology, 2014; 171(8):2191-2205
Publisher: Wiley-Blackwell
Issue Date: 2014
ISSN: 0007-1188
1476-5381
Statement of
Responsibility: 
H Muyderman and T Chen
Abstract: Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disease characterized by the selective death of upper and lower motor neurons which ultimately leads to paralysis and ultimately death. Pathological changes in ALS are closely associated with pronounced and progressive changes in mitochondrial morphology, bioenergetics and calcium homeostasis. Converging evidence suggests that impaired mitochondrial function could be pivotal in the rapid neurodegeneration of this condition. In this review, we provide an update of recent advances in understanding mitochondrial biology in the pathogenesis of ALS and highlight the therapeutic value of pharmacologically targeting mitochondrial biology to slow disease progression.
Keywords: Amyotrophic lateral sclerosis; mitochondria; SOD-1; TDP-43; therapeutic; cell death
Rights: © 2013 The British Pharmacological Society
RMID: 0030050083
DOI: 10.1111/bph.12476
Grant ID: http://purl.org/au-research/grants/nhmrc/1023780
Appears in Collections:Animal and Veterinary Sciences publications

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