Table 3.
Results of regressions analyses of the interaction effect of amyloid deposition and rs671 polymorphism on brain cortical thickness, only showing significant regions.
Regions | Estimatea | Standard errora | Unadjusted P | FDR corrected P |
---|---|---|---|---|
Lt. cuneus | − 0.143 | 0.049 | 0.004 | 0.043 |
Lt. pars opercularis | − 0.162 | 0.047 | 0.001 | 0.038 |
Lt. pars triangularis | − 0.134 | 0.045 | 0.004 | 0.043 |
Lt. rostral middle frontal | − 0.162 | 0.049 | 0.001 | 0.038 |
Lt. superior parietal | − 0.145 | 0.045 | 0.002 | 0.038 |
Lt. insula | − 0.186 | 0.066 | 0.005 | 0.047 |
Rt. inferior parietal | − 0.152 | 0.055 | 0.006 | 0.048 |
Rt. pars triangularis | − 0.163 | 0.055 | 0.004 | 0.043 |
Rt. superior parietal | − 0.139 | 0.048 | 0.005 | 0.045 |
FDR, false discovery rate; APOE, apolipoprotein E; CDR, clinical dementia rating.
Adjusted for age, sex, education year, total intracranial volume, APOE-ε4 carrier status, lifetime drinking status, Framingham general cardiovascular risk score, CDR sum of box, white matter hyperintensity score of peripheral and deep white matter.
aValues from amyloid deposition and rs671 polymorphism interaction term in multiple regression model.