4.5 Article

Conditional deletion of Id2 or Notch1 in oligodendrocyte progenitor cells does not ameliorate disease outcome in SOD1G93A mice

Journal

NEUROBIOLOGY OF AGING
Volume 68, Issue -, Pages 1-4

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2018.03.026

Keywords

Amyotrophic lateral sclerosis; Oligodendrocytes; Id2; Notch1; Differentiation

Funding

  1. Fund for Scientific Research Flanders (FWO)
  2. University of Leuven [GOA/11/014, C14/17/107]
  3. Interuniversity Attraction Poles Programme of the Belgian Federal Science Policy Office [P7/16]
  4. European Research Council (ERC grant) [340429]
  5. ALS Liga (Belgium)
  6. Agency for Innovation, Science and Technology in Flanders (IWT)
  7. E von Behring Chair for Neuromuscular and Neurodegenerative Disorders
  8. Laevers Fund for ALS Research
  9. University of Leuven
  10. European Research Council (ERC) [340429] Funding Source: European Research Council (ERC)

Ask authors/readers for more resources

Oligodendrocytes are essential for structural and trophic support of motor axons. Their impairment has been implicated in amyotrophic lateral sclerosis (ALS), a neurodegenerative disorder of motor neurons. Oligodendrocyte progenitor cells fail to differentiate into mature oligodendrocytes and thereby jeopardize the health of motor neurons. Here, we report that oligodendrocytic ablation of inhibitor of DNA binding 2 (Id2) or Notch receptor 1 (Notch1), 2 negative master modulators of oligodendrocyte differentiation, fails to alleviate oligodendrocyte dysfunction or alter disease outcome in a murine model of ALS. Our data suggest that these inhibitors are not suitable targets for intervention in ALS. (C) 2018 The Authors. Published by Elsevier Inc.

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