Amyloid β-protein oligomers upregulate the β-secretase, BACE1, through a post-translational mechanism involving its altered subcellular distribution in neurons

Background β-Site amyloid precursor proteincleaving enzyme 1 ( BACE1) is a membrane-bound aspartyl protease that initiates amyloidβ-protein (Aβ) generation. Aberrant elevation of BACE1levels in brains of Alzheimer’s disease (AD) patients may involve Aβ. In the present study, we used a neuron culture model system to investigate the effects of Aβ on BACE1expression as well as the underlying mechanisms.