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Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis
05:55

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Published on: December 1, 2023

Glutamate and multiple sclerosis.

M Frigo1, M G Cogo, M L Fusco

  • 1Department of Neurology, S. Gerardo Hospital, Monza (MB), Italy.

Current Medicinal Chemistry
|February 7, 2012
PubMed
Summary
This summary is machine-generated.

Multiple sclerosis (MS) is increasingly recognized as involving early axonal damage. Excessive glutamate release by immune cells in MS plaques suggests new therapeutic targets beyond inflammation.

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Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Multiple sclerosis (MS) traditionally viewed as inflammatory demyelination.
  • Early research focused on inflammation and oligodendrocyte damage.
  • Axonal loss and neurodegeneration are now recognized early in MS.

Purpose of the Study:

  • Investigate the role of glutamate in MS pathogenesis.
  • Identify cellular sources of glutamate release in MS lesions.
  • Explore glutamate modulation as a therapeutic strategy for MS.

Main Methods:

  • Review of preclinical studies in experimental allergic encephalomyelitis.
  • Analysis of post-mortem MS patient tissues.
  • In vivo studies in MS patients.

Main Results:

  • Evidence suggests excessive glutamate release at demyelination and axonal degeneration sites.
  • Infiltrating leukocytes and activated microglia are likely sources of glutamate.
  • Findings are supported by both animal models and human studies.

Conclusions:

  • Glutamate dysregulation is implicated in MS neurodegeneration.
  • Modulating glutamate release, transport, or receptors may offer new MS therapies.
  • Future treatments could target excitotoxicity in MS.