Sorting Out Presenilins in Alzheimer's Disease

Mutations in the presenilins that cause familial Alzheimer's disease alter the activity of these proteases to increase generation of an aggregation-prone isoform of the amyloid beta-peptide (A beta). How these mutations do so has been unclear. Sannerudet al. now show that regulation of subcellular localization plays a central role, advancing our understanding of the cell biology of Alzheimer's disease.