AD diagnosis and criterion count, and further, examine whether novel loci emerged for individual criteria. To identify common variants associated with these phenotypes, a GWAS was performed in the European American (EA, n=1,114 families; “EA GWAS”) subsample of COGA, followed by a trans-ancestral genome-wide meta-analysis of the EA and African American (AA; N=585 families) subsamples. GWS (p<5E-8) findings were tested for replication in three independent datasets (Study of Addiction: Genetics and Environment (SAGE)22, Alcohol Dependence GWAS in European and African Americans (Yale-Penn)21, and the Australian Twin-family Study of Alcohol Use Disorder (OZALC)23, which included EA (OZ-ALC, SAGE) and AA (SAGE, Yale-Penn) individuals. Polygenic risk scores (PRS) were created from the COGA EA GWAS and used to predict AD in EAs from SAGE and OZ-ALC. We also performed gene based analyses using COGA EA GWAS. Lastly, to probe the potential neural correlates of the GWS variants associated with aspects of AD, we tested whether GWS variants identified in the primary (DSM-IV AD), secondary (AD criterion count) or tertiary (individual criteria) analyses were associated with two reward-related neural phenotypes, one within a subset of young individuals from COGA 24and another within the independent Duke Neurogenetics Study 25. The overall design of this
