Enhanced axonal response of mitochondria to demyelination offers neuroprotection: implications for multiple sclerosis.

ABSTRACT: Axonal loss is the key pathological substrate of neurological disability in demyelinating disorders, including multiple sclerosis (MS). However, the consequences of demyelination on neuronal and axonal biology are poorly understood. The abundance of mitochondria in demyelinated axons in MS raises the possibility that increased mitochondrial content serves as a compensatory response to demyelination. Here, we show that upon demyelination mitochondria move from the neuronal cell body to the demyelinated axon, increasing axonal mitochondrial content, which we term the axonal response of mitochondria to demyelination (ARMD). However, following demyelination axons degenerate before the homeostatic ARMD reaches its peak. Enhancement of ARMD, by targeting mitochondrial biogenesis and mitochondria

SUBMITTER: Licht-Mayer S 

PROVIDER: S-EPMC7360646 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature