| Literature DB >> 15122701 |
Bart Dermaut1, Samir Kumar-Singh, Sebastian Engelborghs, Jessie Theuns, Rosa Rademakers, Jos Saerens, Barbara A Pickut, Karin Peeters, Marleen van den Broeck, Krist'l Vennekens, Stephen Claes, Marc Cruts, Patrick Cras, Jean-Jacques Martin, Christine Van Broeckhoven, Peter Paul De Deyn.
Abstract
Familial forms of frontotemporal dementia (FTD) with tauopathy are mostly caused by mutations in the gene encoding the microtubule-associated protein tau (MAPT). However, rare forms of familial tauopathy without MAPT mutations have been reported, suggesting other tauopathy-related genetic defects. Interestingly, two presenilin 1 (PS1) mutations (Leu113Pro and insArg352) recently have been associated with familial FTD albeit without neuropathological confirmation. We report here a novel PS1 mutation in a patient with Pick-type tauopathy in the absence of extracellular beta-amyloid deposits. The mutation is predicted to substitute Gly-->Val at codon position 183 (Gly183Val) and to affect the splice signal at the junction of the sixth exon and intron. Further clinical-genetic investigation showed a positive family history of FTD-like dementia and suggested that Gly183Val is associated with a phenotypically heterogeneous neurodegenerative disorder. Our results suggest PS1 as a candidate gene for Pick-type tauopathy without MAPT mutations.Entities:
Mesh:
Substances:
Year: 2004 PMID: 15122701 DOI: 10.1002/ana.20083
Source DB: PubMed Journal: Ann Neurol ISSN: 0364-5134 Impact factor: 10.422