Functional and Celluar Assessment of Limited Remyelination in the Cuprizone Model

Abstract

The promotion of remyelination after chronic or prolonged episodes of demyelination is an important therapeutic goal for demyelinating diseases. The leading cause of demyelination in humans is multiple sclerosis (MS). This thesis work focused on a mouse model of MS to examine cellular and molecular mechanisms that may cause limited remyelination after chronic demyelination. Cuprizone, a neurotoxicant, was used to induce experimental demyelination. This model mimics the effects of acute and chronic time courses of demyelinating disease progression.

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Document Details

Document Type
Technical Report
Publication Date
Jan 01, 2012
Accession Number
AD1013100

Entities

People

  • Norah E. Hibbits

Organizations

  • Uniformed Services University of the Health Sciences

Tags

DTIC Thesaurus Topics

  • Brain
  • Brain Injuries
  • Cell Physiological Processes
  • Cells
  • Cellular Structures
  • Central Nervous System
  • Cerebral Cortex
  • Demyelinating Diseases
  • Disease Attributes
  • Genetics
  • Multiple Sclerosis
  • Nervous System
  • Neuroglia
  • Peptide Growth Factors
  • Proteins
  • Statistical Analysis
  • Stem Cells

Fields of Study

  • Medicine
  • Psychology

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