Forman M S, Mufson E J, Leurgans S, Pratico D, Joyce S, Leight S, Lee V M-Y, Trojanowski J Q
Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, 422 Curie Blvd., 605B Stellar-Chance Building, Philadelphia, PA 19104, USA.
Neurology. 2007 Mar 6;68(10):757-63. doi: 10.1212/01.wnl.0000256373.39415.b1.
Mild cognitive impairment, hypothesized to be prodromal Alzheimer disease (AD), shows abundant senile plaques and neurofibrillary tangles, but its biochemical correlates remain undefined.
Biochemical profiles of Abeta, tau, alpha-synuclein, and oxidative pathologies were characterized in middle frontal gyrus, inferior parietal cortex, and entorhinal cortex in postmortem frozen brains from subjects diagnosed antemortem with no cognitive impairment, mild cognitive impairment, or AD.
Insoluble Abeta and tau, as well as tissue isoprostanes, from each brain region analyzed did not correlate with the clinical diagnosis proximate to death, but insoluble Abeta and 8,12-iso-iPF(2alpha)-VI levels from gray matter of all brain regions correlated strongly with the burden of AD pathology, whereas insoluble tau did not.
The biochemical alterations in cortical tau, Abeta, and isoprostane do not reflect the onset of clinical dementia.
轻度认知障碍被认为是阿尔茨海默病（AD）的前驱阶段，其特征为大量老年斑和神经原纤维缠结，但其生化相关因素仍不明确。
对生前被诊断为无认知障碍、轻度认知障碍或AD的受试者的死后冰冻大脑中的额中回、顶下叶皮质和内嗅皮质进行β淀粉样蛋白（Aβ）、tau蛋白、α-突触核蛋白的生化分析以及氧化病理特征分析。
所分析的每个脑区中的不溶性Aβ和tau蛋白以及组织异前列腺素与临近死亡时的临床诊断无关，但所有脑区灰质中的不溶性Aβ和8,12-异前列腺素F2α-VI（8,12-iso-iPF(2α)-VI）水平与AD病理负担密切相关，而不溶性tau蛋白则不然。
皮质tau蛋白、Aβ和异前列腺素的生化改变并不反映临床痴呆的发病情况。
