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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
Progression in multiple sclerosis is associated with low endogenous NCAM.
Sharmilee Gnanapavan1, Peggy Ho, Wendy Heywood
1Department of Neuroimmunology, Institute of Neurology, London, UK. s.gnanapavan@ucl.ac.uk
Journal of Neurochemistry
|March 19, 2013
Summary
Neural cell adhesion molecule (NCAM) depletion after demyelination may drive multiple sclerosis (MS) progression. Reduced NCAM levels in chronic MS suggest a loss of regenerative capacity, impacting CNS repair.
Area of Science:
- Neuroscience
- Cell Biology
- Immunology
Background:
- Multiple sclerosis (MS) is a central nervous system (CNS) disorder involving demyelination and neurodegeneration.
- While early MS shows signs of remyelination and repair, the adult CNS regenerative capacity is debated.
- Neural cell adhesion molecule (NCAM) is crucial for axonal growth, guidance, and fasciculation.
Purpose of the Study:
- To investigate the role of NCAM in multiple sclerosis (MS) disease progression.
- To examine NCAM levels in both in vitro and in vivo models of MS.
Main Methods:
- Utilized in vitro and in vivo models simulating MS conditions.
- Quantified NCAM levels over time in healthy and diseased states.
Main Results:
- In healthy CNS, NCAM levels naturally decrease over time.
- Following demyelination in MS, NCAM levels decrease acutely.
- NCAM levels remain significantly reduced in chronic MS stages.
Conclusions:
- NCAM depletion is associated with MS disease progression.
- Reduced NCAM may impair axonal repair and regeneration in the CNS.
- Targeting NCAM could offer a therapeutic strategy for MS.
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