| Literature DB >> 27782105 |
Mathilde Nizon1, Benjamin Cogne1, Jean-Michel Vallat2, Madeleine Joubert3, Jean-Michel Liet4, Laure Simon5, Marie Vincent1, Sébastien Küry1, Pierre Boisseau1, Sébastien Schmitt1, Sandra Mercier1, Claire Bénéteau1, Catherine Larrose6, Marianne Coste6, Xénia Latypova1, Yann Péréon7, Jean-Marie Mussini3, Stéphane Bézieau1, Bertrand Isidor8.
Abstract
Homozygous frameshift variants in CNTNAP1 have recently been reported in patients with arthrogryposis and abnormal axon myelination. In two brothers with severe congenital hypotonia and foot deformities, we identified compound heterozygous variants in CNTNAP1, reporting the first causative missense variant, p.(Cys323Arg). Motor nerve conductions were markedly decreased. Nerve microscopical lesions confirmed a severe hypomyelinating process and showed loss of attachment sites of the myelin loops on the axons, which could be a characteristic of Caspr loss-of-function. We discuss the pathophysiology of the myelination process and we propose to consider this disorder as a congenital hypomyelinating neuropathy.Entities:
Mesh:
Substances:
Year: 2016 PMID: 27782105 PMCID: PMC5159775 DOI: 10.1038/ejhg.2016.142
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246