摘要
The amyloid hypothesis of Alzheimer's disease (AD) pathogen- esis maintains that the key event is the production of specific C-terminal amyloid-β (Aβ) peptides following the abnormal proteolytic cleavage of the amyloid precursor protein (Vassar and Citron, 2000).
The amyloid hypothesis of Alzheimer's disease (AD) pathogen- esis maintains that the key event is the production of specific C-terminal amyloid-β (Aβ) peptides following the abnormal proteolytic cleavage of the amyloid precursor protein (Vassar and Citron, 2000).