Cortical biochemistry in MCI and Alzheimer disease: Lack of correlation with clinical diagnosis
Document Type
Article
Abstract
OBJECTIVE: Mild cognitive impairment, hypothesized to be prodromal Alzheimer disease (AD), shows abundant senile plaques and neurofibrillary tangles, but its biochemical correlates remain undefined. METHODS: Biochemical profiles of Aβ, tau, α-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. RESULTS: Insoluble Aβ and tau, as well as tissue isoprostanes, from each brain region analyzed did not correlate with the clinical diagnosis proximate to death, but insoluble Aβ and 8,12-iso-iPF2α-VI levels from gray matter of all brain regions correlated strongly with the burden of AD pathology, whereas insoluble tau did not. CONCLUSIONS: The biochemical alterations in cortical tau, Aβ, and isoprostane do not reflect the onset of clinical dementia. ©2007AAN Enterprises, Inc.
Publication Date
3-1-2007
Publication Title
Neurology
ISSN
00283878
Volume
68
Issue
10
First Page
757
Last Page
763
PubMed ID
17339583
Digital Object Identifier (DOI)
10.1212/01.wnl.0000256373.39415.b1
Recommended Citation
Forman, M. S.; Mufson, E. J.; Leurgans, S.; Pratico, D.; Joyce, S.; Leight, S.; Lee, V. M.Y.; and Trojanowski, J. Q., "Cortical biochemistry in MCI and Alzheimer disease: Lack of correlation with clinical diagnosis" (2007). Translational Neuroscience. 1764.
https://scholar.barrowneuro.org/neurobiology/1764