Table 1.
Top markers with P<0.000001 from GWAS study in 1831 AD cases and 1764 controls (Meta-analysis for Pfizer, ADNI and GenADA)a.
Table 2.
Association test results for previously identified variants in CR1, PICALM and CLU from three independent sample sets.
Figure 1.
Manhattan plots for GWAS association meta-analysis results combining.
a) Pfizer, ADNI, GenADA; b) plus top marker results in the QFP replication set. The line indicates genome wide significance level. Top markers at the APOE locus were removed in the plots to improve resolution for the other markers.
Figure 2.
Multiple variants at the BIN1 locus are strongly associated with AD.
A) Meta-analysis for all sample sets (including Pfizer, ADNI, GenADA, Harold and QFP) at the chr2 region (500 kb upstream and downstream of BIN1). SNPs rs744373, rs12989701 and rs7561528 are all strongly associated with disease status below the genome-wide significance level. B) Pairwise LD structure (r2) calculated in Haploview using HapMap genotype data (phase III) in 60 unrelated CEPH samples (gene structures were shown using the UCSC genome browser for the hg18 assembly). While rs744373 and rs7561528 are in strong LD, limited LD exists between rs12989701 and rs744373 (r2 = 0.01 in HapMap samples and r2 = 0.05 in Pfizer data set).
Table 3.
Two variants at the BIN1 locus are associated with Alzheimer's disease susceptibility below the genome-wide significance level with limited LD between them.
Table 4.
Pathway Analysis Results in Three Independent Sample setsa.
Table 5.
AD Progression Analysis for validated variants in AD susceptibilitya.