How to successfully apply animal studies in experimental allergic encephalomyelitis to research on multiple sclerosis

Ann Neurol. 2006 Jul;60(1):12-21. doi: 10.1002/ana.20913.

Abstract

In their Point of View entitled "Experimental Allergic Encephalomyelitis: A Misleading Model of Multiple Sclerosis," Sriram and Steiner(1) wrote, "The most disappointing aspect of EAE [experimental allergic encephalomyelitis] as a potential model for MS is its almost total inability to point toward a meaningful therapy or therapeutic approach for MS." Actually, EAE has led directly to the development of three therapies approved for use in multiple sclerosis (MS): glatiramer acetate, mitoxantrone, and natalizumab. Several new approaches to MS are in clinical trials based on positive indications in preclinical work relying on EAE. New clues to the pathogenesis of MS and new potential surrogate markers for MS are shown from research involving EAE when it is critically coupled with actual findings in MS. There are pitfalls in overreliance on the EAE model, or on any animal model for any human disease. Nevertheless, over the past 73 years, the EAE model has proved itself remarkably useful for aiding research on MS.

Publication types

  • Comment
  • Review

MeSH terms

  • Animals
  • Disease Models, Animal*
  • Encephalomyelitis, Autoimmune, Experimental / pathology
  • Encephalomyelitis, Autoimmune, Experimental / physiopathology*
  • Encephalomyelitis, Autoimmune, Experimental / therapy
  • Humans
  • Multiple Sclerosis / pathology
  • Multiple Sclerosis / physiopathology*
  • Multiple Sclerosis / therapy