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Promoting remyelination through cell transplantation therapies in a model of viral-induced neurodegenerative disease

期刊

DEVELOPMENTAL DYNAMICS
卷 248, 期 1, 页码 43-52

出版社

WILEY
DOI: 10.1002/dvdy.24658

关键词

demyelination; virus; remyelination; neural precursor cells; multiple sclerosis

资金

  1. National Institutes of Health (NIH) [R01 NS041249, R01 NS074987]
  2. National Multiple Sclerosis Society Collaborative Research Center grant [RG 4925]
  3. Ray & Tye Noorda Foundation
  4. NIH [R01 AI121945, 5T32NS082174]
  5. California Institute for Regenerative Medicine (CIRM) [RM1-01717, CL1-00502, TR3-05603]

向作者/读者索取更多资源

Multiple sclerosis (MS) is a central nervous system (CNS) disease characterized by chronic neuroinflammation, demyelination, and axonal damage. Infiltration of activated lymphocytes and myeloid cells are thought to be primarily responsible for white matter damage and axonopathy. Several United States Food and Drug Administration-approved therapies exist that impede activated lymphocytes from entering the CNS thereby limiting new lesion formation in patients with relapse-remitting forms of MS. However, a significant challenge within the field of MS research is to develop effective and sustained therapies that allow for axonal protection and remyelination. In recent years, there has been increasing evidence that some kinds of stem cells and their derivatives seem to be able to mute neuroinflammation as well as promote remyelination and axonal integrity. Intracranial infection of mice with the neurotropic JHM strain of mouse hepatitis virus (JHMV) results in immune-mediated demyelination and axonopathy, making this an excellent model to interrogate the therapeutic potential of stem cell derivatives in evoking remyelination. This review provides a succinct overview of our recent findings using intraspinal injection of mouse CNS neural progenitor cells and human neural precursors into JHMV-infected mice. JHMV-infected mice receiving these cells display extensive remyelination associated with axonal sparing. In addition, we discuss possible mechanisms associated with sustained clinical recovery. Developmental Dynamics 248:43-52, 2019. (c) 2018 Wiley Periodicals, Inc.

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