Biomarkers and evolution in Alzheimer disease

被引:33
作者
Rapoport, Stanley I. [1 ]
Nelson, Peter T. [2 ]
机构
[1] NIA, Brain Physiol & Metab Sect, NIH, Bethesda, MD 20892 USA
[2] Univ Kentucky, Div Neuropathol, Dept Pathol, Sanders Brown Ctr Aging, Lexington, KY 40536 USA
关键词
Alzheimer; Evolution; Brain; Biomarker; Association; Cortex; Metabolism; Neuroplasticity; HUMAN BRAIN; ARACHIDONIC-ACID; METABOLIC RATES; DEMENTIA; GLUCOSE; PROGRESSION; ASSOCIATION; MESSENGER; ATROPHY; LIFE;
D O I
10.1016/j.pneurobio.2011.07.006
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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. Published by Elsevier Ltd.
引用
收藏
页码:510 / 513
页数:4
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