These single locus results point to shared pathobiology between AD and PD. Although we cannot exclude the possibility that other genes at this chromosome 17 locus are the pathologically relevant genes, our data are biologically plausible and consistent with prior experimental evidence establishing the role of MAPT in neurodegenerative diseases. 29 The pleiotropic variant we found, rs393152, tags the H1 haplotype at the MAPT locus5, which has been associated with a number of tauopathies including corticobasal degeneration (CBD), progressive supranuclear palsy (PSP), and PD. 5,30 Furthermore, broadly consistent with a prior study 31, our results suggest non-extensive, non-polygenic pleiotropy between AD and PD localized to the MAPT cluster on chromosome 17.
