Nature Communications (Aug 2018)

Targeting myelin lipid metabolism as a potential therapeutic strategy in a model of CMT1A neuropathy

  • R. Fledrich,
  • T. Abdelaal,
  • L. Rasch,
  • V. Bansal,
  • V. Schütza,
  • B. Brügger,
  • C. Lüchtenborg,
  • T. Prukop,
  • J. Stenzel,
  • R. U. Rahman,
  • D. Hermes,
  • D. Ewers,
  • W. Möbius,
  • T. Ruhwedel,
  • I. Katona,
  • J. Weis,
  • D. Klein,
  • R. Martini,
  • W. Brück,
  • W. C. Müller,
  • S. Bonn,
  • I. Bechmann,
  • K. A. Nave,
  • R. M. Stassart,
  • M. W. Sereda

DOI
https://doi.org/10.1038/s41467-018-05420-0
Journal volume & issue
Vol. 9, no. 1
pp. 1 – 14

Abstract

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Charcot–Marie–Tooth disease 1A (CMT1A) is a peripheral demyelinating disease. Here, the authors demonstrate in a rodent model of CMT1A that Schwann cells have impairments in lipid biosynthesis, and that restoring lipids via diet can reverse the dysmyelinating phenotype in these animals.