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dc.contributor.authorJiang, Zhen
dc.contributor.authorWang, Wenzhang
dc.contributor.authorPerry, George
dc.contributor.authorZhu, Xiongwei
dc.contributor.authorWang, Xinglong
dc.date.accessioned2015-09-01T17:05:01Z
dc.date.available2015-09-01T17:05:01Z
dc.date.issued2015-07-29
dc.identifier.citationTranslational Neurodegeneration. 2015 Jul 29;4(1):14
dc.identifier.urihttp://dx.doi.org/10.1186/s40035-015-0037-x
dc.identifier.urihttp://hdl.handle.net/10724/31722
dc.description.abstractAbstract Amyotrophic lateral sclerosis (ALS) is the most common motor neuron disease characterized by progressive loss of motor neurons in the brainstem and spinal cord. Currently, there is no cure or effective treatment for ALS and the cause of disease is unknown in the majority of ALS cases. Neuronal mitochondria dysfunction is one of the earliest features of ALS. Mitochondria are highly dynamic organelles that undergo continuous fission, fusion, trafficking and turnover, all of which contribute to the maintenance of mitochondrial function. Abnormal mitochondrial dynamics have been repeatedly reported in ALS and increasing evidence suggests altered mitochondrial dynamics as possible pathomechanisms underlying mitochondrial dysfunction in ALS. Here, we provide an overview of mitochondrial dysfunction and dynamic abnormalities observed in ALS, and discuss the possibility of targeting mitochondrial dynamics as a novel therapeutic approach for ALS.
dc.titleMitochondrial dynamic abnormalities in amyotrophic lateral sclerosis
dc.typeJournal Article
dc.date.updated2015-07-29T18:19:34Z
dc.language.rfc3066en
dc.rights.holderJiang et al.


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