School of Psychology, Cardiff University, Park Place, Cardiff CF10 3AT, UK.
Biochem Soc Trans. 2011 Aug;39(4):902-9. doi: 10.1042/BST0390902.
The present review summarizes converging evidence from animal and human studies that an early target of amyloid pathology is synaptic activity in the DG (dentate gyrus)/CA3 network. We briefly review the computational significance of the DG/CA3 network in the encoding of episodic memory and present new evidence that the CA3/DG pattern of activation is compromised in a mouse model of amyloid pathology. In addition, we present a new behavioural method to test the prediction that amyloid-related synaptic pathology will disrupt the formation of an integrated episodic-like (what, where and when) memory in mice.
本综述总结了来自动物和人类研究的趋同证据,表明淀粉样蛋白病理学的早期靶标是 DG(齿状回)/CA3 网络中的突触活动。我们简要回顾了 DG/CA3 网络在情景记忆编码中的计算意义,并提出了新的证据表明,在淀粉样蛋白病理学的小鼠模型中,CA3/DG 的激活模式受到了损害。此外,我们还提出了一种新的行为学方法来检验这样一个预测,即与淀粉样蛋白相关的突触病理学将破坏小鼠形成整合的情景样(什么、哪里和何时)记忆的能力。