Can we switch production of toxic Aβ oligomers to neuroprotective Aβ monomers to allow synapse regeneration?
Clive Bate
摘要：Alzheimer'sdisease (AD) is a complex neurological disor-der characterized by a progressive dementia. The amyloid hypothesis states that pathogenesis is driven by the accumu-lation of amyloid β (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 and in vivo. However, the amyloid hypothesis is not universally accepted; critics pointed out poor correlations between con-centrations of Aβ in the brain and clinical disease and that, although numerous compounds reduced the production of Aβ in animal models, few had any clinical benefit in AD pa-tients. The failure of Aβ-lowering therapies in translational research has resulted in important modifications of the amy-loid hypothesis.
机标关键词：animal models
论文发表日期：2017-01-01
在线出版日期：2025-08-15（本平台首次上网日期，不代表文献的发表时间）
页数：2( 1437-1438 )