J Neurosci Res 2001 Oct;66(1):122-34
Karolinska Institute, NEUROTEC, Division of Geriatric Medicine, KFC, NOVUM, Huddinge, Sweden.
Presenilins (PSs) are mutated in a majority of familial Alzheimer disease (FAD) cases. Mutated PSs may cause FAD by a number of pro-apoptotic mechanisms, or by regulating gamma-secretase activity, a protease involved in beta-amyloid precursor protein processing to the neurotoxic beta-amyloid peptide. Besides their normal endoproteolytic processing, PSs are substrates for caspases, being cleaved to alternative N-terminal and C-terminal fragments. Read More