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MeSH Review

Demyelinating Diseases

 
 
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Disease relevance of Demyelinating Diseases

 

Psychiatry related information on Demyelinating Diseases

 

High impact information on Demyelinating Diseases

  • We now demonstrate that mice devoid of Pmp22 are retarded in the onset of myelination and develop abundant sausage-like hypermyelination structures (tomacula) at a young age followed by severe demyelination, axonal loss and functional impairment [10].
  • Absence of MHC class II molecules reduces CNS demyelination, microglial/macrophage infiltration, and twitching in murine globoid cell leukodystrophy [11].
  • A deletion of MBP sequences in the genome of shiverer mice was also demonstrated. cDNAs for MBP will allow molecular investigation of the role this gene plays in both dysmyelinating and demyelinating diseases, as well as questions of MBP biosynthesis [12].
  • These findings demonstrate that lymphocytic cells reactive to myelin basic protein are present in the spinal fluid during active demyelinating disease; and that these cells may be more reactive than peripheral blood lymphocytes [13].
  • Thus, autoimmune responses to sulfatide and other lipids are present in individuals with multiple sclerosis and in EAE, and may contribute to the pathogenesis of autoimmune demyelination [14].
 

Chemical compound and disease context of Demyelinating Diseases

 

Biological context of Demyelinating Diseases

 

Anatomical context of Demyelinating Diseases

 

Gene context of Demyelinating Diseases

 

Analytical, diagnostic and therapeutic context of Demyelinating Diseases

References

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