A Novel Stress-Activated Inhibitor of Myelination

Abstract

In Multiple Sclerosis (MS) myelin and axons are damaged. At the beginning of the disease, the brain can repair itself by remyelination of damaged axons. With time, however, the repair ability of the brain deteriorates, and remyelination is no longer efficient or sometimes even possible. We discovered a novel inhibitor or remyelination that is present in MS plaques and we will test if it can be targeted to promote remyelination and protect axons. So far, we have discovered that this novel inhibitor delays the ability of oligodendrocyte progenitors (the precursors of the cells that will make myelin) to proliferate, migrate and differentiate. We are currently studying the molecular mechanisms by which the inhibitors exert these effects, because this may reveal novel ways to promote myelination. In addition, we have discovered that this inhibitor accelerate also remyelination after injury, using a toxin that deplete myelin-forming cells in an in-vivo model. These latest findings confirm that our novel inhibitors could be relevant to promote remyelination after a demyelination attack in Multiple Sclerosis patients.

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Document Details

Document Type
Technical Report
Publication Date
Jul 01, 2020
Accession Number
AD1108433

Entities

People

  • Leandro Marziali
  • Maria L. Feltri

Organizations

  • University at Buffalo

Tags

DTIC Thesaurus Topics

  • Ablation
  • Abstracts
  • Acquisition
  • Biological Sciences
  • Biomedical Research
  • Brain
  • Cecum
  • Cells
  • Department Of Defense
  • Engineering
  • Governments
  • Humanities
  • Local Governments
  • Medical Personnel
  • Microscopes
  • Multiple Sclerosis
  • Nervous System
  • Neuroglia
  • New York
  • Peripheral Nervous System
  • Professional Development
  • Standards
  • Students
  • Training

Fields of Study

  • Medicine

Readers

  • Immunology and Pathology
  • Medical Imaging.