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Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histocompatibility glycoprotein HLA-DR
Abstract
HLA-DR is a class II cell surface glycoprotein of the human histocompatibility complex usually expressed on the surface of cells that are simultaneously presenting foreign antigen to T-lymphocytes. Using immunohistochemical procedures with two specific monoclonal antibodies to HLA-DR, HLA-DR-positive reactive microglia were found in gray matter throughout the cortex of postmortem brains of patients with senile dementia of the Alzheimer type (SDAT) and were particularly concentrated in the areas of senile plaque formation. Double immunostaining with antibodies to glial fibrillary acidic protein (GFAP) showed that the HLA-DR-positive cells were different from the reactive astrocytes although the occasional positively staining giant astrocyte was also seen. Small numbers of resting microglia were HLA-DR-positive in white matter of both normal and SDAT brains. The SDAT cases also had reduced cortical choline acetyltransferase (ChAT) levels. In the 11 brains studied, the number of hippocampal HLA-DR-positive cells was positively correlated with the numbers of plaques and negatively correlated with average cortical ChAT.
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“AD is accompanied by activation of microglia and astrocytes1,2 that affects the clearance and production of Aβ42,3,4 development and propagation of tau pathology,5 exacerbates neurodegeneration, and influences disease progression and severity.6,7”
From CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease (2018) · cites this paper as [1]
In the citing paper
“Reactive gliosis and neural inflammation are hallmarks of AD4,122–125.”
From Microglial signatures and their role in health and disease (2018) · cites this paper as [122]
In the citing paper
“Microglia in AD have long been known to acquire what is typically considered a “reactive” morphology, with short, thick, and poorly ramified processes [67–69].”
From Microglial dysfunction in brain aging and Alzheimer's disease (2014) · cites this paper as [69]
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Metadata
- Authors
- McGeer, P. L., Itagaki, S., Tago, H., & McGeer, E. G.
- Affiliations
- University of British Columbia (CA)
- Corresponding author
- McGeer, Patrick L.
- ORCID
- McGeer, Patrick L.
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1987-08
- Volume
- 79
- Issue
- 1-2
- Pages
- 195-200
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2074274825
- Cited by
- 836
- References
- 9
- Citations by year
- 2026: 7 · 2025: 19 · 2024: 24 · 2023: 36 · 2022: 32 · 2021: 30 · 2020: 40 · 2019: 31 · 2018: 26 · 2017: 28 · 2016: 21 · 2015: 27 · 2014: 34 · 2013: 27 · 2012: 27
- FWCI
- 14.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- reactive microglia, HLA-DR, senile dementia of the Alzheimer type, Alzheimer's disease, amyloid plaques, glial fibrillary acidic protein, astrocytes, choline acetyltransferase, hippocampus, neuroinflammation
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Cerebral Cortex, Hippocampus, HLA-D Antigens, HLA-DR Antigens, Humans, Neuroglia
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