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 is known to be involved in the breakdown of the blood-brain barrier.
“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]
The Discussion (page not supplied) reports that some CD163-positive microglia coincided with fibrinogen leakage, an indication of blood–brain barrier breakdown. It suggests that vascular compromise might allow CD163-positive macrophages to enter the brain, but does not establish that CD163 itself contributes to the breakdown or that such a role is known. (LLM, conf=0.86)
Experimental — accuracy not yet measuredCD163 is expressed exclusively on perivascular macrophages in the brain under normal conditions, as well as peripheral cells of monocyte lineage.
“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]
The Discussion describes CD163 as generally considered a perivascular-macrophage marker and reports that expression in neurologically normal controls was restricted to those macrophages. The Results qualify the exclusivity claim: in 12 of 16 control cases, staining also appeared in meningeal and choroid-plexus macrophages. The Results also describe CD163 as a marker specific for monocytes, supporting the lineage part of the claim. (LLM, conf=0.86)
Experimental — accuracy not yet measuredPey et al. found higher levels of CD163 staining in the hippocampus, as well as the frontal and occipital cortices.
“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]
CD163 is a hub gene of MG-M4.
“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]
The Discussion describes CD163 as a marker of deactivation and phagocytosis, and the Results examine CD163-positive microglia. Neither passage identifies MG-M4 or assesses whether CD163 is a hub gene; searches for MG-M4 and gene-network terminology found no such passage in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredIncreased expression of CD163, associated with non-microglia myeloid cells, has been observed in the brains of PD patients.
“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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- 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
- Health Sciences › Medicine › Physiology › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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