Our results suggest that some polygenic liability underlying SRE-T and AD is common but also highlight that each phenotype is likely to be influenced by unique genetic factors. For instance, the current strongest signal for AD, rs1229984 in ADH1B (Walters et al., 2018), was not associated at genomewide significant levels to SRE-T (EA p= 0.00027; AA p=0.019; rs2066702, strongest signal in AA, p=0.012). Similarly, the most significant variant for SRE-T in chromosome 11, rs10647170, was not associated with AD (p>0.18 in COGA-AA, COGA-EA, and COGA-AA-EA). Thus, the genetic variants associated with SRE and those relating to AD are likely to only modestly overlap. For example, the AD risk is associated with high impulsivity and sensation seeking, low conscientiousness, and the risk for some psychiatric disorders (e.g., schizophrenia), characteristics that have little, if any, links to LR.
