β淀粉样蛋白（1-42）抑制 LTP 是通过一种涉及半胱天冬酶-3、Akt1 和 GSK-3β的信号通路介导的。
Aβ(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3β.
机构信息
Henry Wellcome Laboratories for Integrative Neuroscience and Endocrinology, School of Clinical Sciences, Faculty of Medicine and Dentistry, University of Bristol, Bristol, UK.
出版信息
Nat Neurosci. 2011 May;14(5):545-7. doi: 10.1038/nn.2785. Epub 2011 Mar 27.
Amyloid-β(1-42) (Aβ) is thought to be a major mediator of the cognitive deficits in Alzheimer's disease. The ability of Aβ to inhibit hippocampal long-term potentiation provides a cellular correlate of this action, but the underlying molecular mechanism is only partially understood. We found that a signaling pathway involving caspase-3, Akt1 and glycogen synthase kinase-3β is an important mediator of this effect in rats and mice.
淀粉样蛋白β（1-42）（Aβ）被认为是阿尔茨海默病认知缺陷的主要介质。Aβ 抑制海马长时程增强的能力为这种作用提供了一个细胞相关性，但潜在的分子机制仅部分被理解。我们发现，涉及半胱天冬酶-3、Akt1 和糖原合酶激酶-3β的信号通路是大鼠和小鼠中这种作用的重要介导物。
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