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Neurosci Lett. 2019 Sep 25;710:132932. doi: 10.1016/j.neulet.2017.06.051. Epub 2017 Jun 28.

Mitochondria in neuroinflammation - Multiple sclerosis (MS), leber hereditary optic neuropathy (LHON) and LHON-MS.

Author information

1
Department of Clinical Neuroscience & MRC Mitochondrial Biology Unit, University of Cambridge, UK. Electronic address: dmb78@cam.ac.uk.
2
Department of Clinical Neuroscience & MRC Mitochondrial Biology Unit, University of Cambridge, UK. Electronic address: pfc25@cam.ac.uk.

Abstract

Mitochondrial dysfunction is associated with neuroinflammation and neurodegenerative disease, but its role as a driver in these processes is uncertain. Understanding the pathogenesis of inherited mitochondrial disorders may help us to uncover mechanisms involved during acquired mitochondrial dysfunction. We review the mechanisms of mitochondrial dysfunction in Leber's hereditary optic neuropathy and multiple sclerosis and discuss shared clinical and molecular features in both conditions. Targeting mitochondrial pathways involved in inflammation or apoptosis may be a possible therapeutic approach in multiple sclerosis.

KEYWORDS:

Harding’s disease; LHON-MS; Leber’s hereditary optic neuropathy; Mitochondria; Multiple sclerosis; Neurodegeneration; Neuroinflammation

PMID:
28668384
DOI:
10.1016/j.neulet.2017.06.051
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