Abstract |
Alzheimer's disease (AD) is the most common dementing illness and is pathologically characterized by deposition of the 40-42 amino acid peptide, amyloid-beta (Abeta), as senile plaques. It is well documented that brain inflammatory mechanisms mediated by reactive glia are activated in response to Abeta plaques. A number of reports further suggest that T-cells are activated in AD patients, and that these cells exist both in the periphery and as infiltrates in the brain. We explore the potential role of T-cells in the AD process, a controversial area, by reviewing reports that show disturbed activation profiles and/or altered numbers of various subsets of T-cells in the circulation as well as in the AD brain parenchyma and in cerebral amyloid angiopathy. We also discuss the recent Abeta immunotherapy approach vis-à-vis the activated, autoaggressive T-cell infiltrates that contributed to aseptic meningoencephalitis in a small percentage of patients, and present possible alternative approaches that may be both efficacious and safe. Finally, we explore the use of mouse models of AD as a system within which to definitively test the possible contribution of T-cells to AD pathogenesis.
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Authors | Terrence Town, Jun Tan, Richard A Flavell, Mike Mullan |
Journal | Neuromolecular medicine
(Neuromolecular Med)
Vol. 7
Issue 3
Pg. 255-64
( 2005)
ISSN: 1535-1084 [Print] United States |
PMID | 16247185
(Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
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Topics |
- Alzheimer Disease
(immunology, pathology, therapy)
- Cerebral Amyloid Angiopathy
(immunology, pathology)
- Humans
- Immunity, Innate
- Immunotherapy
- Lymphocyte Activation
- Microglia
(immunology)
- Plaque, Amyloid
(immunology, pathology)
- T-Lymphocytes
(immunology)
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