Presenilin dysfunction leads to memory and plasticity defects

Impairment in memory formation and early defects in dendritic and synaptic function are among the earliest changes in mice lacking both presenilin genes, Ps1 and Ps2, which are implicated in familial Alzheimer's disease (FAD). These findings reveal an additional pathogenetic mechanism independent of amyloid and suggest that therapies being developed to block presenilin function in FAD may do more harm than good.