Kozin S A, Barykin E P, Mitkevich V A, Makarov A A
Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, Moscow, 119991, Russia.
Biochemistry (Mosc). 2018 Sep;83(9):1057-1067. doi: 10.1134/S0006297918090079.
Drug development for the treatment of Alzheimer's disease (AD) has been for a long time focused on agents that were expected to support endogenous β-amyloid (Aβ) in a monomeric state and destroy soluble Aβ oligomers and insoluble Aβ aggregates. However, this strategy has failed over the last 20 years and was eventually abandoned. In this review, we propose a new approach to the anti-amyloid AD therapy based on the latest achievements in understanding molecular causes of cerebral amyloidosis in AD animal models.
长期以来,治疗阿尔茨海默病(AD)的药物研发一直聚焦于有望支持处于单体状态的内源性β淀粉样蛋白(Aβ)并破坏可溶性Aβ寡聚体和不溶性Aβ聚集体的药物。然而,在过去20年里,这一策略失败了,最终被放弃。在本综述中,我们基于对AD动物模型中脑淀粉样变性分子病因的最新认识,提出了一种抗淀粉样蛋白AD治疗的新方法。