| Literature DB >> 25834054 |
Dinesh C Joshi1, Chuan-Li Zhang1, Tien-Min Lin1, Anchal Gusain2, Melissa G Harris3, Esther Tree1, Yewin Yin1, Connie Wu1, Zu-Hang Sheng4, Robert J Dempsey2, Zsuzsanna Fabry3, Shing Yan Chiu5.
Abstract
The demyelinating disease multiple sclerosis (MS) has an early inflammatory phase followed by an incurable progressive phase with subdued inflammation and poorly understood neurodegenerative mechanism. In this study, we identified various parallelisms between progressive MS and the dysmyelinating mouse model Shiverer and then genetically deleted a major neuron-specific mitochondrial anchoring protein Syntaphilin (SNPH) from the mouse. Prevailing evidence suggests that deletion of SNPH is harmful in demyelination. Surprisingly, SNPH deletion produces striking benefits in the Shiverer by prolonging survival, reducing cerebellar damage, suppressing oxidative stress, and improving mitochondrial health. In contrast, SNPH deletion does not benefit clinical symptoms in experimental autoimmune encephalomyelitis (EAE), a model for early-phase MS. We propose that deleting mitochondrial anchoring is a novel, specific treatment for progressive MS.Entities:
Keywords: axonal degeneration; mitochondria; multiple sclerosis; oxidative stress; syntaphilin
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Year: 2015 PMID: 25834054 PMCID: PMC4381002 DOI: 10.1523/JNEUROSCI.3859-14.2015
Source DB: PubMed Journal: J Neurosci ISSN: 0270-6474 Impact factor: 6.167