Although genome-wide association studies (GWAS) have successfully located various genetic variants susceptible to Alzheimer’s Disease (AD), it is still unclear how specific variants interact with genes and tissues to elucidate pathologies associated with AD. Summary-data-based Mendelian Randomization (SMR) addresses this problem through an instrumental variable approach that integrates data from independent GWAS and expression quantitative trait locus (eQTL) studies in order to infer a causal effect of gene expression on a trait.