| Literature DB >> 26932191 |
Alessia Micalizzi1,2, Andrea Poretti3,4, Marta Romani1, Monia Ginevrino1, Tommaso Mazza1, Chiara Aiello5, Ginevra Zanni5, Bastian Baumgartner6, Renato Borgatti7, Knut Brockmann8, Ana Camacho9, Gaetano Cantalupo10, Martin Haeusler11, Christiane Hikel12, Andrea Klein3, Giorgia Mandrile13, Eugenio Mercuri14, Dietz Rating15, Romina Romaniello7, Filippo Maria Santorelli16, Mareike Schimmel17, Luigina Spaccini18, Serap Teber19, Arpad von Moers20, Sarah Wente8, Andreas Ziegler21, Andrea Zonta13, Enrico Bertini5, Eugen Boltshauser3, Enza Maria Valente1,22.
Abstract
Cerebellar dysplasia with cysts and abnormal shape of the fourth ventricle, in the absence of significant supratentorial anomalies and of muscular involvement, defines recessively inherited Poretti-Boltshauser syndrome (PBS). Clinical features comprise non-progressive cerebellar ataxia, intellectual disability of variable degree, language impairment, ocular motor apraxia and frequent occurrence of myopia or retinopathy. Recently, loss-of-function variants in the LAMA1 gene were identified in six probands with PBS. Here we report the detailed clinical, neuroimaging and genetic characterization of 18 PBS patients from 15 unrelated families. Biallelic LAMA1 variants were identified in 14 families (93%). The only non-mutated proband presented atypical clinical and neuroimaging features, challenging the diagnosis of PBS. Sixteen distinct variants were identified, which were all novel. In particular, the frameshift variant c.[2935delA] recurred in six unrelated families on a shared haplotype, suggesting a founder effect. No LAMA1 variants could be detected in 27 probands with different cerebellar dysplasias or non-progressive cerebellar ataxia, confirming the strong correlate between LAMA1 variants and PBS.Entities:
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Year: 2016 PMID: 26932191 PMCID: PMC4913877 DOI: 10.1038/ejhg.2016.19
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246