| Literature DB >> 26145164 |
Afef Achouri-Rassas1, Nadia Ben Ali2, Saloua Fray2, Sondes Hadj Fredj3, Meriem Kechaou2, Nouria Oudiaa Zakraoui2, Aroua Cherif2, Slim Chabbi2, Nadia Anane2, Taieb Messaoud3, Riadh Gouider4, Samir Belal2.
Abstract
A minority of Alzheimer disease (AD) patients begin presenting symptoms before the age of 65 years. A familial aggregation is often found in this group of early-onset AD, and, in a subset of families, the pattern of inheritance is consistent with autosomal dominant inheritance. Fully penetrant variants in amyloid precursor protein, presenilin 1 (PSEN1), and presenilin 2 are the only causative mutations reported for autosomal dominant AD. This study is to explore the PSEN1 gene mutation in a Tunisian familial Alzheimer's disease. The patient in this family showed a novel missense mutation in exon 4 of the PSEN1 gene (complementary DNA 248T>C), altering isoleucine to threonine at 83 position. Because the change occurred in conserved domains of this gene, and cosegregated with affected family member, we suggested that this change may have a mutagenic and probably pathogenic effect.Entities:
Keywords: Early-onset Alzheimer's disease; PSEN 1 mutation; Tunisian family
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Year: 2015 PMID: 26145164 DOI: 10.1016/j.neurobiolaging.2015.06.007
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673