Journal
NEUROBIOLOGY OF AGING
Volume 28, Issue 12, Pages 1821-1833Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2006.08.014
Keywords
MHC class II; microglia; inflammation; dementia; amyloid beta; T cell
Categories
Funding
- NIA NIH HHS [P30 AG19610, R01 AG023173, AG16573, AG00538, RF1 AG020241, AG 020241, P01 AG000538, P01 AG000538-229001, AG 023173, P30 AG019610, P50 AG016573, R01 AG020241] Funding Source: Medline
- NINDS NIH HHS [NS 050895, R01 NS050895] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available