Genome-wide scan of copy number variation in late-onset Alzheimer's disease.


Autoria(s): Heinzen, EL; Need, AC; Hayden, KM; Chiba-Falek, O; Roses, AD; Strittmatter, WJ; Burke, JR; Hulette, CM; Welsh-Bohmer, KA; Goldstein, DB
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.