Exploration of a Novel Molecular Brake for Remyelination in MS

Abstract

This research study explores ways to enhance myelin repair. The premise upon which the research is founded is that the signaling molecule, Csk, acts as an endogenous suppressor of myelin repair. We have been exploring the possibility that the AMPK pathway is key component of the Csk-induced brake to myelin repair. We have activated AMPK signaling following myelin damage and preliminary indications are that AMPK activation promotes myelin health and/or repair. We also found that AMPK activation enhances oligodendrocyte differentiation from oligodendrocyte progenitor cells using rodent cultures. We have further found that AMPK activation in mice aids in myelin repair. Lastly, we have found that AMPK activation promotes metabolic alterations in developing oligodendrocytes, and likely represents, at least in part, an important mechanism to drive enhanced myelin repair. This last hypothesis will form the basis for our next study.

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Document Details

Document Type
Technical Report
Publication Date
Oct 01, 2020
Accession Number
AD1118315

Entities

People

  • Holly Colognato
  • Mohanlall Narine

Organizations

  • Stony Brook University

Tags

Communities of Interest

  • Biomedical

DTIC Thesaurus Topics

  • Alzheimer Disease
  • Biomedical Research
  • Brain
  • Cells
  • Energy Production
  • Gene Expression
  • Medical Personnel
  • Metabolism
  • Molecules
  • Multiple Sclerosis
  • Nervous System
  • Neuroglia
  • Nucleotides
  • Professional Development
  • Rate Of Consumption
  • Stem Cells
  • Students

Readers

  • Immunology and Pathology
  • Medical Imaging.