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Phenotypic profile of alternative activation marker CD163 is different in Alzheimer’s and Parkinson’s disease
Open accessAbstract
BACKGROUND: Microglial activation is a pathological feature common to both Alzheimer's and Parkinson's diseases (AD and PD). The classical activation involves release of pro-inflammatory cytokines and reactive oxygen species. This is necessary for maintenance of tissue homeostasis and host defense, but can cause bystander damage when the activation is sustained and uncontrolled. In recent years the heterogeneous nature of microglial activation states in neurodegenerative diseases has become clear and the focus has shifted to alternative activation states that promote tissue maintenance and repair. We studied the distribution of CD163, a membrane-bound scavenger receptor found on perivascular macrophages. CD163 has an immunoregulatory function, and has been found in the parenchyma in other inflammatory diseases e.g. HIV-encephalitis and multiple sclerosis. In this study, we used immunohistochemistry to compare CD163 immunoreactivity in 31 AD cases, 27 PD cases, and 16 control cases. Associations of microglia with pathological hallmarks of AD and PD were investigated using double immunofluorescence. RESULTS: Parenchymal microglia were found to be immunoreactive for CD163 in all of the AD cases, and to a lesser extent in PD cases. There was prominent staining of CD163 immunoreactive microglia in the frontal and occipital cortices of AD cases, and in the brainstem of PD cases. Many of them were associated with Aß plaques in both diseases, and double staining with CD68 demonstrates their phagocytic capability. Leakage of fibrinogen was observed around compromised blood vessels, raising the possibility these microglia might have originated from the periphery. CONCLUSIONS: Increase in microglia's CD163 immunoreactivity was more significant in AD than PD, and association of CD163 immunoreactive microglia with Aβ plaques indicate microglia's attraction towards extracellular protein pathology, i.e. extracellular aggregates of Aβ as compared to intracellular Lewy Bodies in PD. Double staining with CD163 and CD68 might point towards their natural inclination to phagocytose plaques. Fibrinogen leakage and compromise of the blood brain barrier raise the possibility that these are not resident microglia, but systemic macrophages infiltrating the brain.
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“CD163, a hub gene of MG-M4, is known to be involved in the breakdown of the blood-brain barrier.53,54”
From hdWGCNA identifies co-expression networks in high-dimensional transcriptomics data (2023) · cites this paper as [54]
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“CD163 is a hemoglobin-haptoglobulin scavenger receptor that is considered to be expressed exclusively on perivascular macrophages in the brain under normal conditions, as well as peripheral cells of monocyte lineage [38, 56].”
From Loss of homeostatic microglial phenotype in CSF1R-related Leukoencephalopathy (2020) · cites this paper as [38]
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“Like Dal Bianco et al.20 Pey et al.120 also found higher levels of CD163 staining in the hippocampus, as well as the frontal and occipital cortices.”
From Markers of microglia in post-mortem brain samples from patients with Alzheimer’s disease: a systematic review (2018) · cites this paper as [120]
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“CD163, a hub gene of MG-M4, is known to be involved in the breakdown of the blood-brain barrier.53,54”
From hdWGCNA identifies co-expression networks in high-dimensional transcriptomics data (2023) · cites this paper as [54]
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“Increased expression of proteins associated with non-microglia myeloid cells, such as CD163, has been observed in the brains of PD patients.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [227]
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Metadata
- Authors
- Pey, P., Pearce, R. K., Kalaitzakis, M. E., Griffin, W. S. T., & Gentleman, S. M.
- Affiliations
- Imperial College London (GB)
- University of Arkansas for Medical Sciences (US)
- Corresponding author
- Pey, Peixuan
- Gentleman, Steve M
- Venue
- Acta Neuropathologica Communications
- Published
- 2014-02-14
- Volume
- 2
- Issue
- 1
- Pages
- 21-21
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC3940003
- OpenAlex
- W2147311470
- Cited by
- 128
- References
- 71
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 10 · 2023: 18 · 2022: 14 · 2021: 11 · 2020: 16 · 2019: 11 · 2018: 8 · 2017: 9 · 2016: 7 · 2015: 5
- FWCI
- 3.64
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Parkinson's UK (G0909, J-1402)
- Imperial College London
- National Institutes of Health (AG12411)
- National Institute on Aging (AG 12411, P01AG012411)
- 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
- CD163, Alzheimer's disease, Parkinson's disease, amyloid plaques, Lewy bodies, CD68, blood-brain barrier, perivascular macrophages, phagocytosis, neuroinflammation
- MeSH terms
- CD68 Molecule, CD163 Antigen, Aged, Aged, 80 and over, Alzheimer Disease, Brain, Calcium-Binding Proteins, Cell Count, DNA-Binding Proteins, Female, Fibrinogen, Humans, Macrophages, Male, Membrane Glycoproteins, Microfilament Proteins, Middle Aged, Neurologic Examination, Parkinson Disease, Receptors, Cell Surface, Receptors, Immunologic, Antigens, Differentiation, Myelomonocytic, Antigens, CD, Amyloid beta-Peptides, Microglia, Plaque, Amyloid
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