Mutations in the two presenilin genes (PS1, PS2) account for the majority of early-onset
familial Alzheimer's disease (FAD) cases. Converging evidence from a variety of
experimental systems, including fibroblasts from FAD patients and transgenic animals,
indicates thatPS1 mutations modulate intracellular calcium signaling pathways. Despite the
potential relevance of these changes to the pathogenesis of FAD, a comparable effect for
PS2 has not yet been demonstrated experimentally. We examined the effects of wild-type …