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

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.

Bibliographic Details
Main Authors: 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
Format: Article
Language:English
Published: Nature Publishing Group 2018-08-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-05420-0
Description
Summary: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.
ISSN:2041-1723