Amyloid, memory and neurogenesis.
Amyloid, memory and neurogenesis.
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淀粉样蛋白、记忆和神经发生。
DOI：
10.1016/j.expneurol.2007.03.006
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发表时间：
2007
影响因子：
5.3
通讯作者：
Morgan,Dave
中科院分区：
文献类型：
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作者：
Morgan,Dave
淀粉样蛋白沉积的转基因小鼠模型一直显示出在某些学习和记忆任务中表现受损。这篇文章是由张等人撰写的。(2006)在淀粉样蛋白沉积的小鼠模型中展示了齿状回神经发生的减少，这与淀粉样蛋白的沉积有关，而不是转基因的过度表达。神经发生在记忆的形成中至少起到了促进作用，而记忆的本质才刚刚开始显现。因此，似乎有理由认为，在淀粉样前体蛋白转基因小鼠的淀粉样沉积模型中发现的记忆缺陷，至少部分是由于海马神经发生率降低所致。还讨论了与阿尔茨海默病痴呆患者记忆丧失的可能关系。
Transgenic mouse models of amyloid deposition consistently demonstrate impaired performance on certain tasks of learning and memory. The article by Zhang et al. (2006) demonstrates reductions in dentate gyrus neurogenesis in a murine model of amyloid deposition which is linked to the deposition of amyloid and not overexpression of transgenes. Neurogenesis plays at least a facilitatory role in the formation of memory, the nature of which is only beginning to emerge. Thus, it seems reasonable to propose that the memory deficits found in the amyloid precursor protein transgenic mouse models of amyloid deposition result, at least in part, from reduced rates of hippocampal neurogenesis. The possible relationship to memory loss in Alzheimer's dementia is also discussed.