Study of the interaction of unaggregated and aggregated amyloid β protein (10-21) with outward potas

• 作 者: ZHANG ChaoFeng FAN Li YANG Pin
• 机 构: Key Laboratory of Chemical Biology and Molecular Engineering of Ministry of Education
• 出 处: 中国科学B辑（英文版）
• 发表日期: 2004年期
• 关键词: potassium channel amyloid β protein (10-21) Zn2+ alzheimer's disease

Metal ion-induced aggregation of Aβinto insoluble plaques is a central factor in Alzheimer's disease. Zn2+ is the only physiologically available transition metal ion responsible for aggregating Aβ at pH 7.4. To make it clear that the neurotoxicity of Zn2+-induced aggregation of Aβ on neurons is the key to understand Aβ mechanism of action further. In this paper, we choose Aβ (10-21) as the model fragment to research hippocampal CA1 pyramidal neurons. For the first time, we adopt the combination of spectral analysis with patch-clamp technique for the preliminary study of the mutual relations of Zn2+, Aβ and ion channel from the cell level. The following expounds upon the effects and mode of action of two forms (unaggregated and aggregated) of Aβ (10-21) on hippocampus outward potassium channel three processes (activation, inactivation and reactivation). It also shows the molecular mechanics of AD from the channel level. These results are significant for the further study of Aβ nosogenesis and the development of new types of target drugs for the treatment of AD.