Journal
NEUROBIOLOGY OF AGING
Volume 68, Issue -, Pages 1-4Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2018.03.026
Keywords
Amyotrophic lateral sclerosis; Oligodendrocytes; Id2; Notch1; Differentiation
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Funding
- Fund for Scientific Research Flanders (FWO)
- University of Leuven [GOA/11/014, C14/17/107]
- Interuniversity Attraction Poles Programme of the Belgian Federal Science Policy Office [P7/16]
- European Research Council (ERC grant) [340429]
- ALS Liga (Belgium)
- Agency for Innovation, Science and Technology in Flanders (IWT)
- E von Behring Chair for Neuromuscular and Neurodegenerative Disorders
- Laevers Fund for ALS Research
- University of Leuven
- European Research Council (ERC) [340429] Funding Source: European Research Council (ERC)
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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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