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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
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Neurodegeneration in multiple sclerosis
Gabrielle M Mey1, Kedar R Mahajan1,2, Tara M DeSilva1
1Department of Neurosciences, Lerner Research Institute, Cleveland Clinic Foundation, and Case Western Reserve University, Cleveland, Ohio, USA.
Wires Mechanisms of Disease
|August 10, 2022
Summary
Axonal loss in multiple sclerosis (MS) drives permanent disability. New research explores neuroprotective strategies to combat neurodegeneration and promote repair in the central nervous system (CNS).
Area of Science:
- Neuroscience
- Immunology
- Pathology
Background:
- Multiple sclerosis (MS) is a complex CNS disease causing axonal loss and neurodegeneration.
- Current immunomodulatory therapies manage inflammatory relapses but do not halt progressive disease or cure MS.
- Axonal degeneration contributes significantly to irreversible neurological deficits in MS patients.
Purpose of the Study:
- To review current understanding of MS pathogenesis, focusing on mechanisms of neurodegeneration.
- To identify early signs of axonal dysfunction and factors contributing to chronic axonal loss.
- To highlight the need for neuroprotective and regenerative strategies for MS treatment.
Main Methods:
- Analysis of data from MS patients, post-mortem studies, and animal models of demyelination.
- Review of proposed MRI and molecular biomarkers for predicting neurodegeneration.
- Examination of early axonal dysfunction indicators like impaired mitochondrial trafficking and synaptic alterations.
Main Results:
- Chronic demyelination and inflammation in the CNS perpetuate axonal loss.
- Impaired remyelination hinders repair processes.
- Early axonal dysfunction includes mitochondrial, structural, and synaptic changes.
Conclusions:
- Understanding MS pathogenesis is crucial for developing neuroprotective therapies.
- Regenerative and neuroprotective strategies are essential for preserving axonal integrity.
- Early intervention is critical to rescue axonal function and mitigate CNS atrophy in MS.
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