Psychotic symptoms occur in∼ 40% of subjects with Alzheimer's disease (AD) and are associated with more rapid cognitive decline and increased functional deficits. They show heritability up to 61% and have been proposed as a marker for a disease subtype suitable for gene mapping efforts. We undertook a combined analysis of three genome-wide association studies (GWASs) to identify loci that (1) increase susceptibility to an AD and subsequent psychotic symptoms; or (2) modify risk of psychotic symptoms in the presence of neurodegeneration caused by AD. In all, 1299 AD cases with psychosis (AD+ P), 735 AD cases without psychosis (AD–P) and 5659 controls were drawn from Genetic and Environmental Risk in AD Consortium 1 (GERAD1), the National Institute on Aging Late-Onset Alzheimer's Disease (NIA-LOAD) family study and the University of Pittsburgh Alzheimer Disease Research Center (ADRC) GWASs. Unobserved genotypes were imputed to provide data on> 1.8 million single-nucleotide polymorphisms (SNPs). Analyses in each data set were completed comparing (1) AD+ P to AD–P cases, and (2) AD+ P cases with controls (GERAD1, ADRC only). Aside from the apolipoprotein E (APOE) locus, the strongest evidence for association was observed in an intergenic region on chromosome 4 (rs753129;‘AD+ PvAD–P’P= 2.85× 10− 7;‘AD+ PvControls’ P= 1.11× 10− 4). SNPs upstream of SLC2A9 (rs6834555, P= 3.0× 10− 7) and within VSNL1 (rs4038131, P= 5.9× 10− 7) showed strongest evidence for association with AD+ P when compared with controls. These findings warrant further investigation in larger, appropriately powered samples in which the presence of psychotic symptoms in AD has been well characterized.