Inflammatory changes parallel the early stages of Alzheimer disease

被引:176
|
作者
Parachikova, A. [1 ]
Agadjanyan, M. G.
Cribbs, D. H.
Blurton-Jones, M.
Perreau, V.
Rogers, J.
Beach, T. G.
Cotman, C. W.
机构
[1] Univ Calif Irvine, Inst Brain Aging & Dementia, Gillespie Neurosci Res Facil 1113, Irvine, CA 92697 USA
[2] Univ Calif Irvine, Coll Med, Dept Neurol, Irvine, CA 92697 USA
[3] Inst Mol Med, Dept Immunol, Huntington Beach, CA 92647 USA
[4] Sun Hlth Res Inst, LJ Roberts Ctr, Sun City, AZ 85351 USA
关键词
MHC class II; microglia; inflammation; dementia; amyloid beta; T cell; CENTRAL-NERVOUS-SYSTEM; GENE-EXPRESSION PROFILE; ANTIINFLAMMATORY DRUG-USE; CLASS-II; SYNAPSE LOSS; T-CELLS; A-BETA; MICROGLIA; BRAIN; PATHOLOGY;
D O I
10.1016/j.neurobiolaging.2006.08.014
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Alzheimer disease (AD) is the most prominent cause of dementia in the elderly. To determine changes in the AD brain that may mediate the transition into dementia, the gene expression of approximately 10,000 full-length genes was compared in mild/moderate dementia cases to non-demented controls that exhibited high AD pathology. Including this latter group distinguishes this work from previous studies in that it allows analysis of early cognitive loss. Compared to non-demented high-pathology controls, the hippocampus of AD cases with mild/moderate dementia had increased gene expression of the inflammatory molecule major histocompatibility complex (MHC) II, as assessed with microarray analysis. MHC II protein levels were also increased and inversely correlated with cognitive ability. Interestingly, the mild/moderate AD dementia cases also exhibited decreased number of T cells in the hippocampus and the cortex compared to controls. In conclusion, transition into AD dementia correlates with increased MHC II+ microglia-mediated immunity and is paradoxically paralleled by a decrease in T cell number, suggesting immune dysfunction. (C) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:1821 / 1833
页数:13
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