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T-Cells in Alzheimer's Disease
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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Systemic immune response, including T-cell immune response, may be involved in the inflammation process of AD.
“increased studies suggest that systemic immune response, including T-cell immune response, may be involved in the inflammation process of AD [152, 153].”
From PKR, the double stranded RNA‐dependent protein kinase as a critical target in Alzheimer's disease (2009) · cites this paper as [153]
Neuroinflammation is a key factor in the development and progression of Alzheimer's disease.
“Neuroinflammation is a key factor in the development and progression of AD [144, 145].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [144]
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Metadata
- Authors
- Town, T., Tan, J., Flavell, R. A., & Mullan, M.
- Affiliations
- Yale University (US)
- University of South Florida (US)
- Howard Hughes Medical Institute (US)
- Roskamp Institute (US)
- Corresponding author
- Mullan, Mike
- Venue
- NeuroMolecular Medicine
- Published
- 2005
- Volume
- 7
- Issue
- 3
- Pages
- 255-264
- ISSN
- 1535-1084 (ISSN-L)
- OpenAlex
- W1992860518
- Cited by
- 183
- References
- 66
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 7 · 2023: 9 · 2022: 12 · 2021: 11 · 2020: 13 · 2019: 11 · 2018: 11 · 2017: 12 · 2016: 7 · 2015: 10 · 2014: 13 · 2013: 15 · 2012: 8
- FWCI
- 3.20
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- NeuroMolecular Medicine (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institutes of Health
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, T cells, amyloid-beta, amyloid plaques, cerebral amyloid angiopathy, neuroinflammation, reactive glia, T cell activation, aseptic meningoencephalitis, amyloid-beta immunotherapy, mouse models of Alzheimer's disease
- MeSH terms
- Alzheimer Disease, Humans, Immunity, Innate, Immunotherapy, Lymphocyte Activation, T-Lymphocytes, Cerebral Amyloid Angiopathy, Microglia, Plaque, Amyloid
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