Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
Geriatr Gerontol Int. 2010 Jul;10 Suppl 1:S169-79. doi: 10.1111/j.1447-0594.2010.00598.x.
One hallmark of Alzheimer's disease (AD) is the accumulation of amyloid beta (Abeta) peptides in the brain; Abeta mainly consists of 42-mer and 40-mer peptides (Abeta42 and Abeta40). Abeta42 plays a more critical role in the pathogenesis of AD because Abeta42 aggregates much faster and is more toxic than Abeta40. Therefore, there is an urgent need to elucidate the mechanism of aggregation and neurotoxicity of Abeta42 to develop therapeutic agents. Here, we introduce the pathological role of Abeta42 in AD and review our recent findings of the structural analysis of Abeta42 using systematic proline replacement, electron spin resonance and solid-state nuclear magnetic resonance, and the new mechanism of neurotoxicity of Abeta42 through the formation of radicals.
阿尔茨海默病（AD）的一个标志是淀粉样β（Abeta）肽在大脑中的积累；Abeta 主要由 42 个和 40 个氨基酸组成的肽（Abeta42 和 Abeta40）。Abeta42 在 AD 的发病机制中起着更关键的作用，因为 Abeta42 聚集速度更快，比 Abeta40 更具毒性。因此，迫切需要阐明 Abeta42 的聚集和神经毒性机制，以开发治疗药物。在这里，我们介绍了 Abeta42 在 AD 中的病理作用，并回顾了我们最近使用系统脯氨酸替换、电子自旋共振和固态核磁共振对 Abeta42 的结构分析的发现，以及通过自由基形成的 Abeta42 新的神经毒性机制。
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