| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 10956841 | Molecular and Cellular Neuroscience | 2005 | 12 Pages |
Abstract
These results are relevant to reveal the molecular function of PMP22 and the pathogenic mechanism of CMT1A. In particular, finding a specific reduction of cntf expression in CMT1A Schwann cells suggests that overexpression of pmp22 significantly affects the ability of Schwann cells to offer a trophic support to the axon, which could be a factor, among other, responsible for the development of axonal atrophy in human and experimental CMT1A.
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Authors
Tiziana Vigo, Lucilla Nobbio, Paul Van Hummelen, Michele Abbruzzese, GianLuigi Mancardi, Nathalie Verpoorten, Kristien Verhoeven, Michael W. Sereda, Klaus-Armin Nave, Vincent Timmerman, Angelo Schenone,