Genome-wide scan of copy number variation in late-onset Alzheimer's disease.
Data(s) |
2010
|
---|---|
Formato |
69 - 77 |
Identificador |
http://www.ncbi.nlm.nih.gov/pubmed/20061627 V7N8Q30275184532 J Alzheimers Dis, 2010, 19 (1), pp. 69 - 77 http://hdl.handle.net/10161/4614 1875-8908 |
Idioma(s) |
ENG en_US |
Relação |
J Alzheimers Dis 10.3233/JAD-2010-1212 Journal of Alzheimers Disease |
Palavras-Chave | #Adult #Aged #Aged, 80 and over #Alzheimer Disease #Apolipoprotein E4 #DNA Copy Number Variations #Female #Genetic Predisposition to Disease #Genetic Variation #Genome-Wide Association Study #Humans #Male #Middle Aged #Polymorphism, Single Nucleotide #Young Adult |
Tipo |
Journal Article |
Cobertura |
Netherlands |
Resumo |
Alzheimer's disease is a complex and progressive neurodegenerative disease leading to loss of memory, cognitive impairment, and ultimately death. To date, six large-scale genome-wide association studies have been conducted to identify SNPs that influence disease predisposition. These studies have confirmed the well-known APOE epsilon4 risk allele, identified a novel variant that influences disease risk within the APOE epsilon4 population, found a SNP that modifies the age of disease onset, as well as reported the first sex-linked susceptibility variant. Here we report a genome-wide scan of Alzheimer's disease in a set of 331 cases and 368 controls, extending analyses for the first time to include assessments of copy number variation. In this analysis, no new SNPs show genome-wide significance. We also screened for effects of copy number variation, and while nothing was significant, a duplication in CHRNA7 appears interesting enough to warrant further investigation. |