MYO18A and Alzheimer disease: By filter retardation assay, we have recently determined that protein aggregates of TPC6A and TIAF1 are present in the hippocampus of normal middle-aged individuals, and the TPC6A/TIAF1 complexes possess increasing amounts of Aβ in AD patients.1 The aggregated TPC6AΔ induces TIAF1 aggregation and activates caspases for causing APP degradation and Aβ generation.