meaning they are not (yet) good at predicting disease risk in individuals — but are useful to understand genetic overlap of SUDs with psychiatric and behavioural traits. Due to the wide range of methods applied and SUD-related traits tested, it is hard to compare studies using different metrics, such as testing PRS on other datasets when the PRS were generated from datasets based on different sample sizes and phenotype definitions. With respect to PRS derived from traits related to alcohol consumption and dependence (e.g., AUDIT-C and AUDIT-P), several associations were observed across traits related to cocaine, amphetamine, and MDMA (3,4-Methylenedioxymethamphetamine; also known as ‘ecstasy’)87 in addition to alcohol use phenotypes assssed in independent cohorts (i.e., alcohol dependence, AUD symptom count, maximum drinks, increased likelihood of AD onset, and ICD-based alcohol-related disorders88,89). In a cross-ancestry analysis, AD PRS derived from Thai and European-American GWAS were associated with AD in Han Chinese, although the effect was mostly due to the contribution of the ALDH2 and ADH1B loci19. Similarly to alcohol-related studies, PRS derived from smoking traits showed associations across traits related to multiple substances (e.g., cocaine, amphetamine, hallucinogens, ecstasy, and cannabis initiation, as well as DSM-5 AUD)87,90,91. For cannabis, PRS derived from
