Please use this identifier to cite or link to this item:
https://hdl.handle.net/2440/106788
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dc.contributor.author | Muyderman, H. | - |
dc.contributor.author | Chen, T. | - |
dc.date.issued | 2014 | - |
dc.identifier.citation | British Journal of Pharmacology, 2014; 171(8):2191-2205 | - |
dc.identifier.issn | 0007-1188 | - |
dc.identifier.issn | 1476-5381 | - |
dc.identifier.uri | http://hdl.handle.net/2440/106788 | - |
dc.description.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. | - |
dc.description.statementofresponsibility | H Muyderman and T Chen | - |
dc.language.iso | en | - |
dc.publisher | Wiley-Blackwell | - |
dc.rights | © 2013 The British Pharmacological Society | - |
dc.source.uri | http://dx.doi.org/10.1111/bph.12476 | - |
dc.subject | Amyotrophic lateral sclerosis; mitochondria; SOD-1; TDP-43; therapeutic; cell death | - |
dc.title | Mitochondrial dysfunction in amyotrophic lateral sclerosis - a valid pharmacological target? | - |
dc.type | Journal article | - |
dc.identifier.doi | 10.1111/bph.12476 | - |
dc.relation.grant | http://purl.org/au-research/grants/nhmrc/1023780 | - |
pubs.publication-status | Published | - |
dc.identifier.orcid | Chen, T. [0000-0002-7681-9632] | - |
Appears in Collections: | Animal and Veterinary Sciences publications Aurora harvest 3 |
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