A mechanistic hypothesis for the impairment of synaptic plasticity by soluble Aβ oligomers from Alzheimer's brain

S. Li, D. J. Selkoe

This review summarized AD brain‐derived soluble Aβ oligomers (principally small, diffusible oligomers) could disrupt synaptic plasticity, by binding to membranes and changing excitatory‐inhibitory balance, perturbing cellular prion protein and mGluR, down‐regulating glutamate transporters, activating cytokines and associated inflammatory mediators, and causing LTP inhibition and LTD facilitation. We synthesize these emerging data into a mechanistic hypothesis for synaptic failure in AD that can be modified as new knowledge is added and specific therapeutics are developed.

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中文翻译：

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发行信息

阿尔茨海默氏症大脑中可溶性Aβ寡聚体损害突触可塑性的机制假说

李S.DJ Selkoe

这篇综述总结了AD脑源性可溶性Aβ低聚物（主要是小的，可扩散的低聚物）可能通过与膜结合并改变兴奋性抑制平衡，扰乱细胞蛋白和mGluR，下调谷氨酸转运蛋白，激活细胞因子及相关物质来破坏突触可塑性。炎症介质，并导致LTP抑制和LTD促进。我们将这些新兴数据合成为AD突触失败的机械假说，可以通过添加新知识和开发特定疗法来对其进行修改。

阅读完整的文章，第583页。