Alzheimer's amyloid story finds its star
Alzheimer's amyloid story finds its star
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DOI：
10.1016/j.molmed.2006.07.002
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发表时间：
2006-09-01
影响因子：
13.6
通讯作者：
Frautschy, Sally A.
中科院分区：
文献类型：
--
作者：
Cole, Greg M.;Frautschy, Sally A.
β-淀粉样多肽(A-beta)在遗传学上被认为是阿尔茨海默病的病因，但淀粉样蛋白沉积成斑块的因果关系受到了质疑。在Lesne及其同事最近的一篇论文中，淀粉样肽在阿尔茨海默病中的有争议的作用得到了强调，他们应用Koch的假设，将一种特定的导致记忆缺陷的寡聚体物种作为导致记忆丧失的中心参与者。这些作者使用转基因小鼠模型来识别一种特定类型的聚集体，这种聚集体出现时存在认知缺陷，并能够将空间记忆缺陷传递给未受损的动物。
beta-Amyloid peptides (A beta) have been genetically implicated as the cause of Alzheimer's disease, but the causality of amyloid deposited as plaques has been challenged. The controversial role of amyloid peptides in Alzheimer's disease has been highlighted in a recent paper from Lesne and colleagues, who applied Koch's postulates to cast a specific memory-deficit-inducing oligomer species as a central player causing memory loss. These authors used a transgenic mouse model to identify a specific type of aggregate that emerges with cognitive deficits and is capable of transmitting a spatial memory defect to unimpaired animals.