Enhanced neuronal degradation of amyloid-β oligomers allows synapse regeneration

摘要

The amyloid hypothesis of Alzheimer’s disease(AD)pathogenesis 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).Aβpeptides self-aggregate and are found in multiple forms from small soluble monomers and oligomers to much larger fibrils and plaques.The soluble Aβoligomers