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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Review: Mitochondria and disease progression in multiple sclerosis
D Mahad1, H Lassmann, D Turnbull
1The Mitochondrial Research Group, University of Newcastle upon Tyne, Newcastle, UK. d.j.mahad@ncl.ac.uk
Neuropathology and Applied Neurobiology
|December 17, 2008
Summary
Mitochondrial dysfunction in demyelinated axons contributes to multiple sclerosis (MS) progression. Targeting mitochondria may offer a therapeutic strategy for MS axonal degeneration.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Multiple sclerosis (MS) is a central nervous system inflammatory demyelinating disease.
- Axonal dysfunction and degeneration are key drivers of MS progression.
Purpose of the Study:
- To review evidence and mechanisms of demyelinated axon degeneration in MS.
- To highlight the role of mitochondria in axonal dysfunction and degeneration in MS.
Main Methods:
- Literature review focusing on mitochondrial roles in demyelinated axons.
- Analysis of evidence linking mitochondrial dysfunction to axonal vulnerability in MS.
Main Results:
- Demyelinated axons exhibit mitochondrial changes and sodium channel redistribution.
- These alterations suggest increased vulnerability to energy deficits.
- Mitochondrial dysfunction is observed in MS lesions and normal-appearing brain matter.
Conclusions:
- Mitochondrial dysfunction is a significant factor in axonal dysfunction and degeneration in MS.
- Mitochondria represent a promising therapeutic target for managing MS progression.
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