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Updated: Jun 24, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

Published on: July 19, 2019

Mitochondrial changes within axons in multiple sclerosis.

Don J Mahad¹, Iryna Ziabreva, Graham Campbell

¹Mitochondrial Research Group, Newcastle University, Framlington Place, Newcastle upon Tyne, NE2 4HH, UK. d.j.mahad@ncl.ac.uk

Brain : a Journal of Neurology

|March 19, 2009

Summary

This summary is machine-generated.

Mitochondrial dysfunction, specifically reduced complex IV activity, contributes to axonal injury and neurological impairment in multiple sclerosis. Inactive lesions show increased mitochondrial mass in some axons, suggesting complex repair mechanisms.

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Published on: February 9, 2020

Area of Science:

Neuroscience
Cell Biology
Pathology

Background:

Multiple sclerosis (MS) is a leading cause of neurological disability in young adults.
Axonal degeneration, linked to energy deficiency, drives MS progression.
Mitochondria are crucial for cellular energy production and calcium regulation.

Purpose of the Study:

To investigate mitochondrial density and function in chronic active and inactive lesions of progressive MS.
To correlate mitochondrial changes with axonal injury markers and immune cell infiltration.

Main Methods:

Immunohistochemistry and histochemistry were used to analyze mitochondria.
Mitochondrial respiratory chain complex IV activity was assessed.
Markers of axonal damage (amyloid precursor protein, SMI32, phosphorylated neurofilament-H) and immune cells were evaluated.

Main Results:

Reduced complex IV activity was observed in demyelinated axons at active lesion edges, despite normal mitochondrial presence.
Strong SMI32 reactivity correlated with decreased complex IV activity and mitochondrial density.
Inactive lesions showed increased complex IV activity and mitochondrial mass in some large demyelinated axons.
Inhibition of complex IV exacerbated glutamate-induced axonal injury in vitro.

Conclusions:

Mitochondrial complex IV defects contribute to axonal injury and dysfunction in progressive MS.
Immune cell activity may influence mitochondrial dysfunction in active lesions.
Chronic demyelinated axons may exhibit compensatory mitochondrial increases in inactive lesions.