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Reviews in the Neurosciences

Editor-in-Chief: Huston, Joseph P.

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Volume 30, Issue 1


Multiple sclerosis pathogenesis: missing pieces of an old puzzle

Reza Rahmanzadeh
  • MS Research Center, Neuroscience Institute, Tehran University of Medical Science, Department of Neurology, Sina Hospital, 1136746911 Tehran, Iran
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
/ Wolfgang Brück / Alireza Minagar / Mohammad Ali Sahraian
  • Corresponding author
  • MS Research Center, Neuroscience Institute, Tehran University of Medical Science, Department of Neurology, Sina Hospital, 1136746911 Tehran, Iran
  • Iranian Center for Neurological Research, Neuroscience Institute, Tehran University of Medical Science, 1136746890 Tehran, Iran
  • Email
  • Other articles by this author:
  • De Gruyter OnlineGoogle Scholar
Published Online: 2018-06-08 | DOI: https://doi.org/10.1515/revneuro-2018-0002


Traditionally, multiple sclerosis (MS) was considered to be a CD4 T cell-mediated CNS autoimmunity, compatible with experimental autoimmune encephalitis model, which can be characterized by focal lesions in the white matter. However, studies of recent decades revealed several missing pieces of MS puzzle and showed that MS pathogenesis is more complex than the traditional view and may include the following: a primary degenerative process (e.g. oligodendroglial pathology), generalized abnormality of normal-appearing brain tissue, pronounced gray matter pathology, involvement of innate immunity, and CD8 T cells and B cells. Here, we review these findings and discuss their implications in MS pathogenesis.

Keywords: degeneration; heterogeneity; inflammation; multiple sclerosis; neuropathology; oligodendrocyte; pathogenesis


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About the article

Received: 2018-01-13

Accepted: 2018-03-30

Published Online: 2018-06-08

Published in Print: 2018-12-19

Citation Information: Reviews in the Neurosciences, Volume 30, Issue 1, Pages 67–83, ISSN (Online) 2191-0200, ISSN (Print) 0334-1763, DOI: https://doi.org/10.1515/revneuro-2018-0002.

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