BACE1 is at the crossroad of a toxic vicious cycle involving cellular stress and β-amyloid production in Alzheimer’s disease

摘要: Alzheimer’s disease (AD) is a complex age-related pathology, the etiology of which has not been firmly delineated. Among various histological stigmata, AD-affected brains display several cellular dysfunctions reflecting enhanced oxidative stress, inflammation process and calcium homeostasis disturbance. Most these alterations are directly or indirectly linked to amyloid β-peptides (Aβ), production, molecular nature biophysical properties likely conditions degenerative process. It particularly noticeable that, in reverse control process, above-described alter Aβ peptides levels. β-secretase βAPP-cleaving enzyme 1 (BACE1) key contributor this cross-talk. This responsible for primary cleavage generating N-terminus “full length” also transcriptionally induced by stresses. review summarizes data linking brain insults AD-like pathology documents role BACE1 at cross-road vicious cycle contributing production.