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Related Experiment Video

Updated: Jun 21, 2026

Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

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Published on: July 19, 2019

Axonal degeneration in multiple sclerosis: the mitochondrial hypothesis.

Kimmy G Su¹, Gary Banker, Dennis Bourdette

¹Oregon Health & Science University, Vollum Institute, L474, 3181 Southwest Sam Jackson Park Road, Portland, OR 97239, USA. suk@ohsu.edu

Current Neurology and Neuroscience Reports

|August 12, 2009

Summary

Mitochondrial failure drives axonal degeneration in multiple sclerosis (MS), a central nervous system disease. Targeting mitochondria offers a promising neuroprotective strategy for MS patients.

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Area of Science:

Neuroscience
Cell Biology
Pathology

Background:

Multiple sclerosis (MS) is a chronic central nervous system disease affecting over 2 million people globally.
While traditionally viewed as inflammatory and demyelinating, MS increasingly involves axonal degeneration, leading to irreversible disability.
Axonal damage occurs throughout MS, with mitochondrial dysfunction implicated as a common mechanism.

Purpose of the Study:

To review the mitochondrial hypothesis of axonal degeneration in multiple sclerosis.
To explore mechanisms linking mitochondrial dysfunction to axonal damage in both acute and progressive MS.
To discuss mitochondria as potential therapeutic targets for neuroprotection in MS.

Main Methods:

Literature review of studies on multiple sclerosis pathogenesis.
Analysis of mechanisms underlying mitochondrial failure in axonal degeneration.
Examination of the role of calcium ions, free radicals, and mitochondrial permeability transition pore.

Main Results:

Mitochondrial failure is a common factor in axonal degeneration across all stages of MS.
Specific mechanisms involve calcium overload, free radical production, and mPTP opening, leading to mitochondrial dysfunction.
Mitochondrial dysfunction impairs axonal transport and results in axonal degeneration.

Conclusions:

Mitochondrial dysfunction is central to axonal degeneration in multiple sclerosis.
Understanding these mechanisms provides insight into MS pathophysiology.
Targeting mitochondrial pathways presents a viable therapeutic strategy for neuroprotection in MS.