Skip to main content
. 2011 Nov 15;1(11):e54. doi: 10.1038/tp.2011.50

Table 2. Candidate variants identified from recent GWAS scans for AD susceptibilitya.

SNP Gene Chr. Position (b.p.) Minor allele frequency Genotype × time interaction nominal P-value Bonferroni corrected P-valueb
Pre-specified
 rs3818361 CLU 8 27 520 436 0.38 0.948 1
 rs3851179 PICALM 11 85 546 288 0.34 0.027 0.108
 rs3818361 CR1 1 205 851 591 0.22 0.933 1
 rs744373 BIN1 2 127 611 085 0.3 0.566 1
             
Post hoc
 rs11767557 EPHA1 7 142 819 261 0.19 0.013 0.065
 rs3865444 CD33 19 56 419 774 0.29 0.439 1
 rs3764650 ABCA7 19 997 520 0.10 0.804 1
 rs610932 MS4A6A 11 59 695 883 0.44 0.840 1
 rs670139 MS4A6A/MS4A4E 11 59 728 371 0.41 0.592 1
 rs9349407 CD2AP 6 47 561 337 NA NA NA

Abbreviations: AD, Alzheimer's disease; CDR-SB, Clinical Dementia Rating-sum of boxes; MMSE, Mini-Mental State Examination; GWAS, genome-wide association studies; NA, not applicable; SNP, single-nucleotide polymorphism.

a

The analysis was performed with experimentally obtained genotype data using change of CDR-SB as end point and a repeated mixed model to adjust for study, baseline age, gender, baseline MMSE, baseline CDR-SB and APOE ɛ4 status (+/−).

b

Variants in CLU, PICALM, CR1 and BIN1 were pre-specified, whereas the other recently reported variants were investigated after the primary analysis.