Annals of neurology · 2004
A novel presenilin 1 mutation associated with Pick's disease but not beta-amyloid plaques.
Клинический случайСравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Dermaut Bart, Kumar-Singh Samir, Engelborghs Sebastian, Theuns Jessie, Rademakers Rosa, Saerens Jos, Pickut Barbara A, Peeters Karin, van den Broeck Marleen, Vennekens Krist'l, Claes Stephen, Cruts Marc, Cras Patrick, Martin Jean-Jacques, Van Broeckhoven Christine, De Deyn Peter Paul
Аннотация
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.