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Alzheimer disease (AD) is characterized by amyloid plaques and neurofibrillary tangles in patients’ brains. Increasing evidence suggests that the abnormal accumulation of amyloid-beta peptides (Aβ), the major component of the amyloid plaques, leads to the development of plaques and tangles and to cognitive dysfunction. Generation of Aβ requires the action of an endopeptidase called β-secretase (BACE1), which cleaves amyloid precursor protein (APP) at the N-terminal end of the Aβ region. Inhibition of BACE1 activity is heralded as one of the most promising strategies for the prevention or treatment of AD.
Endogenous BACE1 is predominantly localized in the late Golgi/trans-Golgi network compartment, but BACE1 may be more likely to process APP …