Biomarkers and evolution in Alzheimer disease.

Biomarkers and evolution in Alzheimer disease.
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DOI:
10.1016/j.pneurobio.2011.07.006
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发表时间:
2011-12
影响因子:
6.7
通讯作者:
Nelson PT
Nelson PT
中科院分区:
医学2区
文献类型:
--
作者:
Rapoport SI;Nelson PT

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在原始人进化过程中迅速扩张的大脑区域及其高度神经可塑性的长轴突连接优先受到阿尔茨海默病的影响。没有完全疾病病理的自然动物模型(神经原纤维缠结和阿尔茨海默病大脑中看到的严重的神经性淀粉样斑块)。生物标志物,如与新皮质相关的葡萄糖代谢降低,长白质束缺陷,RNA神经化学变化,脑脊液中总tau蛋白和高水平的磷酸化tau蛋白,有助于识别MCI和临床前阿尔茨海默病患者,也可能提供关于在类人进化过程中是什么大脑变化导致这种疾病引入的洞察。
Brain regions and their highly neuroplastic long axonal connections that expanded rapidly during hominid evolution are preferentially affected by Alzheimer disease. There is no natural animal model with full disease pathology (neurofibrillary tangles and neuritic amyloid plaques of a severity seen in Alzheimer’s disease brains). Biomarkers such as reduced glucose metabolism in association neocortex, defects in long white matter tracts, RNA neurochemical changes, and high CSF levels of total and phosphorylated tau protein, which are helpful to identify MCI and preclinical Alzheimer disease patients, may also provide insights into what brain changes led to this disease being introduced during hominid evolution.
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