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GWAS Study

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

Heinzen EL, Need AC, Hayden KM et al.

20061627 PubMed ID
GWAS Study Type
699 Participants
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Chapter I

Publication Details

Comprehensive information about this research publication

Authors

HE
Heinzen EL
NA
Need AC
HK
Hayden KM
CO
Chiba-Falek O
RA
Roses AD
SW
Strittmatter WJ
BJ
Burke JR
HC
Hulette CM
WK
Welsh-Bohmer KA
GD
Goldstein DB
Chapter II

Abstract

Summary of the research findings

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.

331 European ancestry cases, 368 European ancestry controls

Chapter III

Study Statistics

Key metrics and study information

699
Total Participants
GWAS
Study Type
No
Replicated
European
Ancestry
Chapter IV

Analysis

Comprehensive review of health and genetic findings

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