Journal
FEBS LETTERS
Volume 592, Issue 7, Pages 1113-1121Publisher
WILEY
DOI: 10.1002/1873-3468.13013
Keywords
demyelination; mitochondria; multiple sclerosis; neurodegeneration; progression
Funding
- National Multiple Sclerosis Society, USA
- Wellcome Trust Institutional Strategic Support Fund
- Multiple Sclerosis Society, UK
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The neuron is the target of inflammatory demyelinating processes in multiple sclerosis (MS). In progressive MS, however, there is a gathering body of evidence indicating that molecular changes converge on mitochondria within neuronal cell bodies. The most reproducible change relates to mitochondrial respiratory chain complex deficiency, which compromises the capacity of neurons to generate ATP. The resulting energy failure state is coupled with an increase in demand for energy by the demyelinated axon, being particularly relevant to the long tracts such as corticospinal tracts with long projection axons. Recent work in our laboratory and that of our collaborators indicates the limited reflection of the mitochondria changes within neurons in experimental disease models. The mitochondrial changes within neuronal compartments are likely to offer novel targets for the improvement in neuronal function in patients with progressive MS.
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