Cortical biochemistry in MCI and Alzheimer disease: lack of correlation with clinical diagnosis

• Published in: Neurology Vol. 68; no. 10; p. 757
• Main Authors: Forman, M S, Mufson, E J, Leurgans, S, Pratico, D, Joyce, S, Leight, S, Lee, V M-Y, Trojanowski, J Q
• Format: Journal Article
• Language: English
• Published: United States 06.03.2007
• Subjects: Aged; Aged, 80 and over; Alzheimer Disease - metabolism; Alzheimer Disease - pathology; Amyloid beta-Peptides - metabolism; Analysis of Variance; Brain Chemistry; Cerebral Cortex - metabolism; Cognition Disorders - metabolism; Cognition Disorders - pathology; Female; Gas Chromatography-Mass Spectrometry - methods; Humans; Immunoassay - methods; Isoprostanes - metabolism; Male; tau Proteins - metabolism
• ISSN: 1526-632X
• 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.