Can we switch production of toxic Aβ oligomers to neuroprotective Aβ monomers to allow synapse regeneration?

摘要

Alzheimer’s disease(AD)is a complex neurological disorder characterized by a progressive dementia.The amyloid hypothesis states that pathogenesis is driven by the accumulation of amyloidβ(Aβ)peptides within the brain(Hardy and Higgins,1992),which have multiple effects including activation of glial cells and synapse degeneration.For many years therapeutic strategies were based upon the discovery of compounds that reduced the production of Aβin vitro