The global outbreak of COVID-19 is linked to long-term neurological complications, including an increased risk of Alzheimer’s disease (AD) among older adults. We investigated whether phenotypes of COVID-19 and AD held pathological connections by analyzing the genetic relationship between them. This study explored the association between AD and polygenic risk scores (PRS) of three COVID-19 phenotypes in European ancestry (EA) and African ancestry (AA) cohorts. PRS-AD associations were determined using logistic regression models adjusted for age, sex, and APOE genotypes. Mendelian randomization (MR) was used to test putative causal relationships between the COVID-19 phenotypes and AD. We also identified overlapping genomic regions between AD and COVID-19 GWASs, and performed a phenome-wide association scan (PheWAS) in the region to identify traits associated with the shared genetic variants. Significant positive associations ( p<0.0167) were found between COVID-19 PRSs and AD in both populations, with the strongest identified in the AA population. However, MR analyses revealed no evidence of a causal effect of COVID-19 phenotypes on AD liability in either ancestry. Exploring this finding further, we identified overlapping genetic associations on chromosome 17 between COVID-19 hospitalization, critical illness, and AD in the EA population. A PheWAS of the rs12373123 and rs199515 SNPs found within the overlapping region revealed multiple significant trait associations ( p<1.05 x10 -5) implicating immune function, psychiatric disorders, and lung function phenotypes. This suggests that while COVID-19 and AD share overlapping polygenic contributions found across multiple traits, they lack a direct connection involving core genes that drive the development of their respective pathologies.