A genetic variant in PLCγ2, which breaks down PI(4,5)P2, protects against AD.Decreased PI(4,5)P2 metabolism via PLCγ2 in PD, increased PI(4,5)P2 in PD substantia nigra.Overexpression of SYNJ1, which hydrolyzes PI(4,5)P2, acts as a risk factor for AD and appears to contribute to plaque pathology and behavioral deficits in mouse models.Mutations in SYNJ1 associated with early-onset PD. Here, SYNJ1 is linked to Alzheimer disease.