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