The DOI matches its Crossref record; 110 of the 112 references it cites were found in a registry or an index; 44 of the 63 sources its claims cite were checked for support.
Beyond Activation: Characterizing Microglial Functional Phenotypes
Open accessAbstract
Classically, the following three morphological states of microglia have been defined: ramified, amoeboid and phagocytic. While ramified cells were long regarded as “resting”, amoeboid and phagocytic microglia were viewed as “activated”. In aged human brains, a fourth, morphologically novel state has been described, i.e., dystrophic microglia, which are thought to be senescent cells. Since microglia are not replenished by blood-borne mononuclear cells under physiological circumstances, they seem to have an “expiration date” limiting their capacity to phagocytose and support neurons. Identifying factors that drive microglial aging may thus be helpful to delay the onset of neurodegenerative diseases, such as Alzheimer’s disease (AD). Recent progress in single-cell deep sequencing methods allowed for more refined differentiation and revealed regional-, age- and sex-dependent differences of the microglial population, and a growing number of studies demonstrate various expression profiles defining microglial subpopulations. Given the heterogeneity of pathologic states in the central nervous system, the need for accurately describing microglial morphology and expression patterns becomes increasingly important. Here, we review commonly used microglial markers and their fluctuations in expression in health and disease, with a focus on IBA1 low/negative microglia, which can be found in individuals with liver disease.
Overview
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Written from the paper’s full text.
TL;DR
This review argues that microglial functional phenotypes cannot be reliably inferred from single morphological or antigenic markers, because markers such as IBA1, TMEM119, P2RY12, CD74, MHCII, and CD68 vary across states and diseases. It highlights IBA1-low/negative microglia, including in individuals with liver disease, and calls for combining morphology, marker panels, and transcriptomic signatures.
Key findings
- Four morphological microglial phenotypes are distinguished—resting, activated, amoeboid, and dystrophic—but IBA1 reliably stains ramified, activated, amoeboid, and dystrophic microglia, so it cannot distinguish functional phenotypes.
- IBA1 loss or decrease is reported in human hippocampus with hepatic pathologies, non-proliferative hepatic encephalopathy, schizophrenia temporal cortex, Huntington’s disease striatum, and Alzheimer’s disease cortex; IBA1-low Alzheimer’s populations showed increased ferritin, CD74, and CD45, while plaque-associated microglia expressed high HLA-DR but much less IBA1.
- TMEM119 was expressed in at least 50% of IBA1-positive human microglia and in 98% of rodent CD45lowCD11b+ cells, but was absent in necrotic cerebral infarctions and demyelinating multiple sclerosis lesions; in Alzheimer’s disease, TMEM119 mRNA was elevated although immunohistochemical analyses showed no difference.
- P2RY12 is specific for parenchymal microglia and downregulated during activation/disease-associated states; CD74 was expressed in all human microglial morphological states; CD68 is a lysosomal/phagocytic marker, and a cluster from 16,096 individual microglial transcriptomes with distinct CD68 upregulation was most enriched for disease-associated microglia genes.
Methods
- Narrative review; the authors review commonly used microglial markers and their expression fluctuations in health and disease, with a focus on IBA1-low/negative microglia found in individuals with liver disease.
- Evidence base consists of cited human and rodent studies using immunohistochemistry, single-cell RNA sequencing, and disease models including Alzheimer’s disease, multiple sclerosis, Parkinson’s disease, schizophrenia, and hepatic encephalopathy.
- Main analysis is a qualitative synthesis of marker expression across morphological states and pathologies; no systematic search strategy or meta-analysis is described.
Limitations
- Stated: associating single markers with a distinct phenotype is difficult because most markers are expressed in several or even all microglial functional states.
- Stated: many studies use IBA1 as the sole microglial marker, so they have not discriminated between a reduction in total microglial numbers and decreased IBA1 expression; the exact function of IBA1 still needs to be elucidated, and species differences are noted, such as CD74 expression in human versus rodent microglia.
- Evident from the text: as a narrative review, it lacks a systematic search, explicit inclusion criteria, and quantitative synthesis, so its conclusions depend on the cited literature and may be subject to selection or reporting bias.
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Claims the paper makes
44 of 63 cited sources checked · 22 supported · 0 flagged · accuracy not yet measured
Every source the paper cites for this claim was checked and supports it.
In the paper
“Even though IBA1 is often characterized as a typical microglial activation marker [8,9,10], it cannot be used to distinguish between functional microglial phenotypes [2].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Supportedcites [2] Walker, 2015, Immune phenotypes of microglia in human neurodegenerative disease: Challenges to detecting mi-croglial polarization in human brains, Alzheimers Res. Ther. source
In “Microglia in human brains,” the paper says IBA-1 identifies all microglia and is not useful for identifying their immune phenotype or polarity. This directly supports the attributed claim. (LLM, conf=0.95)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Following the transient occlusion of the middle cerebral artery (MCA) in rats, the IBA1 staining density and intensity were strongly increased in the ischemic core and the ischemic border zone, compared to the non-affected hemisphere [13].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Supportedcites [13] Michalski, 2017, Delayed histochemical alterations within the neurovascular unit due to transient focal cerebral ischemia and experimental treatment with neurotrophic factors, PLoS ONE source
The Results section, “Vascular and glial alterations in relation to the ischemic lesion in untreated animals,” reports that Iba staining density and intensity were highest in the ischemic core, lower in the border zone, and lower still in the contralateral striatum, with significant differences between regions. This supports increased staining in both ischemic regions relative to the non-affected hemisphere. (LLM, conf=0.91)
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, as we will describe in this review, associating single markers to a distinct phenotype is difficult, since most markers are expressed in several or even all microglial functional states (Figure 1, [2]).”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 1. Introduction
What the sources say
- Partly supportedcites [2] Walker, 2015, Immune phenotypes of microglia in human neurodegenerative disease: Challenges to detecting mi-croglial polarization in human brains, Alzheimers Res. Ther. sourceExperimental — accuracy not yet measured
The Abstract says that widely used microglial markers do not distinguish different phenotypes, and the CD68 section says that both M1- and M2-polarized cells can express CD68. These passages support the difficulty of assigning a phenotype from a single marker, but do not establish that most markers are expressed in several or all functional states. Page numbers are unavailable in our copy. (LLM, conf=0.82)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“While the distribution of microglia varies between different brain regions [11], the expression of allograft inflammatory factor 1 (AIF-1, gene for IBA1) on microglia does not differ between white matter and grey matter [12].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Supportedcites [12] Vlaar, 2019, Regulation of microglial TMEM119 and P2RY12 immunoreactivity in multiple sclerosis white and grey matter lesions is dependent on their inflammatory envi-ronment, Acta Neuropathol. Commun. source
The Results section on primary human microglia states that AIF-1 expression did not differ between microglia derived from white matter and grey matter. This directly supports the attributed comparison; the measurements were made in cultured, tissue-derived microglia. (LLM, conf=0.93)
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In contrast to so-called homeostatic microglial markers, such as transmembrane protein (TMEM-)119 or P2RY12, IBA1 is also expressed by peripheral macrophages [4,5,6,7].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Partly supportedcites [4] Buckman, 2014, Obesity induced by a high-fat diet is associated with increased immune cell entry into the central nervous system, Brain Behav. Immun. sourceExperimental — accuracy not yet measured
Results §3.4 reports that most recruited, donor-derived GFP+ cells in the brain expressed Iba1, supporting the point that IBA1 is not restricted to resident microglia. The paper does not address TMEM119 or P2RY12 or compare their expression with IBA1, so it does not support that part of the sentence. (LLM, conf=0.85)
- Not checked — no full text of the sourcecites [5] 2007, Allograft inflammatory factor-1/Ionized calcium-binding adapter molecule 1 is specifically expressed by most subpopulations of macrophages and spermatids in testis, Cell Tissue Res. source
- Not checked — no full text of the sourcecites [6] Leone, 2006, Characterization of human monocyte-derived mi-croglia-like cells, Glia source
- Not checked — no full text of the sourcecites [7] Sasaki, 2001, Iba1 Is an Actin-Cross-Linking Protein in Macrophages/Microglia, Biochem. Biophys. Res. Commun. source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In contrast, studying the long-term effects of a high-fat, high-carbohydrate diet (HFCD) in the hippocampus of rats, Gzielo et al. [19] showed that the area fraction covered by IBA1-positive cells was reduced after consumption for one year.”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Supportedcites [19] Gzielo, 2016, Long-Term Consumption of High-Fat Diet in Rats: Effects on Microglial and Astrocytic Morphology and Neuronal Nitric Oxide Synthase Expression, Cell. Mol. Neurobiol. source
The Introduction states that the rats received a high-fat, high-carbohydrate diet for 12 months. The Results (Area Fraction) report significantly lower hippocampal Iba1-immunoreactive area fraction in those rats than in controls. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“In fact, we have shown that dystrophic, much more than activated microglia are present in human AD [83,104,107].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 7. CD68
What the sources say
- Supportedcites [83] Streit, 2009, Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in Alzheimer’s disease, Acta Neuropathol. source
The Discussion reports dystrophic microglia accompanying neuritic plaques and says the authors did not observe activated microglia across cases ranging from no to severe AD pathology. This supports the citing sentence’s comparison in human AD. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [104] Streit, 2018, Microglial activation occurs late during preclinical Alzheimer’s disease, Glia source
- Not checked — no full text of the sourcecites [107] Streit, 2020, Dystrophic microglia in late-onset Alzheimer’s disease, Glia source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“CD74 was characterized as a cell surface receptor for the macrophage migration inhibitory factor (MIF, [70,71]).”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 5. CD74
What the sources say
- Supportedcites [70] Farr, 2020, Role of MIF Cytokine/CD74 Receptor Pathway in Protecting Against Injury and Promoting Repair, Front. Immunol. source
The section “CD74 Is A Receptor for MIF Cytokine” states that CD74 was identified as the MIF receptor and that MIF binds its extracellular domain. The “CD74” section also describes CD74 expression on cell surfaces. Page numbers are not provided in the supplied copy. (LLM, conf=0.94)
- Supportedcites [71] Leng, 2003, MIF Signal Transduction Initiated by Binding to CD, J. Exp. Med. source
The Abstract identifies CD74 as a high-affinity binding protein for MIF and reports that MIF binds its extracellular domain. The Discussion describes CD74 as a membrane receptor for MIF and confirms that CD74 is expressed on the cell surface. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“and microglia upregulate HLA-DR in response to IFNγ stimulation [27].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 6. MHCII
What the sources say
- Supportedcites [27] Hendrickx, 2017, Staining of HLA-DR, Iba1 and CD68 in human microglia reveals partially overlapping expression depending on cellular morphology and pathology, J. Neuroimmunol. source
The Introduction explicitly states that microglia upregulate HLA-DR in response to interferon (IFN)-γ stimulation. The claim accurately paraphrases that statement. (LLM, conf=0.95)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“while rodent studies even demonstrated an expression of 98% of CD45lowCD11b+ cells in adult animals [41].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 3. TMEM119
What the sources say
- Supportedcites [41] Bennett, 2016, New tools for studying microglia in the mouse and human CNS, Proc. Natl. Acad. Sci. USA source
In “Custom Anti-Tmem119 Monoclonal Antibodies Specifically Identify Microglia,” the authors report that 98.1 ± 0.6% of CD45loCD11b+ cells were Tmem119+ in adult (P60) mice. This supports the citing sentence’s rounded 98% figure for adult rodents. (LLM, conf=0.94)
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Supported
- It may state two separate claims as one. 15
- Probably not a substantial claim. 3
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Compared with homeostatic microglia, DAM were characterized by the downregulation of AIF1 and homeostatic genes, such as P2RY12, TMEM119, Cx3Cr1, while CD74 and CD68 were upregulated (Supplementary Material in [28]).”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Partly supportedcites [28] Spinrad, 2017, A Unique Microglia Type Associated with Restricting Development of Alzheimer’s Disease, Cell sourceExperimental — accuracy not yet measured
The Results (page unavailable; Figures 1B, 1E, and S1D) report lower P2ry12, Cx3cr1, and Tmem119 expression in DAM than in homeostatic microglia. The passages found do not establish downregulation of AIF1 or upregulation of CD74 and CD68; the paper instead names other upregulated DAM genes, including Apoe, Lpl, and Cst7. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Consistent with these results, experiments investigating the deficiency of TREM2 detected lower transcription levels of IBA1 and a decrease in IBA1-positive microglia. This observation was visible at every timepoint tested and even increased with age [35].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Supportedcites [35] Bodea, 2019, TREM2 triggers microglial density and age-related neuronal loss, Glia source
The Results section reports lower transcription of Aif1, the Iba1-encoding gene, in TREM2 knockout mice, especially at 24 months. It also reports fewer Iba1-positive cells at every investigated time point, with the difference especially pronounced at 24 months. (LLM, conf=0.93)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Recent progress in single-cell deep sequencing methods allowed for more refined differentiation and revealed regional-, age- and sex-dependent differences of the microglial population, and a growing number of studies demonstrate various expression profiles defining microglial subpopulations.”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > Abstract
What the sources say
- Partly supportedcites [28] Spinrad, 2017, A Unique Microglia Type Associated with Restricting Development of Alzheimer’s Disease, Cell sourceExperimental — accuracy not yet measured
The Results report that single-cell RNA-seq identified distinct microglial expression profiles, including disease-associated microglia, and found changes across disease stages and between young and aged mice. They also locate these cells near amyloid plaques, but do not establish broad differences between brain regions. The paper uses sex-matched controls; the passages do not report sex-dependent differences. (LLM, conf=0.88)
- Partly supportedcites [39] Olah, 2020, Single cell RNA sequencing of human microglia uncovers a subset associated with Alzheimer’s disease, Nat. Commun. sourceExperimental — accuracy not yet measured
The Introduction and Results report that single-cell RNA sequencing identified nine human microglial subpopulations with distinct expression profiles. However, the Results say the observed differences between sample sets could not be resolved as effects of age, brain region, sample type, or diagnosis; the cited passages do not establish sex-dependent differences either. (LLM, conf=0.88)
- Partly supportedcites [99] Ayata, 2018, Epigenetic regulation of brain region-specific microglia clearance activity, Nat. Neurosci. sourceExperimental — accuracy not yet measured
The Discussion (page unavailable) reports distinct striatal and cerebellar microglial expression profiles and says single-nucleus RNA sequencing helped assess microglial diversity. The Single nuclei sequencing Methods (page unavailable) specify 4-month-old female mice; although the bulk-sequencing Methods list other ages and sexes, the cited paper does not establish age- or sex-dependent differences through its single-nucleus analysis. (LLM, conf=0.88)
- Partly supportedcites [102] Hammond, 2019, Single-Cell RNA Sequencing of Microglia throughout the Mouse Lifespan and in the Injured Brain Reveals Complex Cell-State Changes, Immunity sourceExperimental — accuracy not yet measured
The Results sections on developmental subpopulations and axon tract–associated microglia report age-dependent transcriptional states and a subpopulation localized to particular brain regions. But the Results section on sex says clustering differed almost not at all between males and females, with only one very small female-enriched cluster; it concludes that diversity was largely unaffected by sex. Thus the sex-dependent part overstates this paper's findings. (LLM, conf=0.90)
- Partly supportedcites [108] Li, 2019, Developmental Heterogeneity of Microglia and Brain Myeloid Cells Revealed by Deep Single-Cell RNA Sequencing, Neuron sourceExperimental — accuracy not yet measured
The Results describe developmental changes in microglial gene expression and distinct microglial clusters; the Discussion reports discovery of the PAM subset. But the Results and Discussion find little transcriptomic variation among classical adult microglia across the regions tested, and STAR Methods state that only male mice were used. This paper therefore does not establish the claimed sex-dependent differences, and its regional finding is more qualified than the claim suggests. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [109] Patir, 2019, A core transcriptional signature of human microglia: Derivation and utility in describing region-dependent alterations associated with Alzheimer’s disease, Glia source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“However, experiments using interferon regulatory factor 8 (IRF8)-deficient microglia [36], showed significantly reduced levels of IBA1, but no deficits in phagocytosis.”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Supportedcites [36] Minten, C., Terry, R., Deffrasnes, C., King, N.J.C., and Campbell, I.L. (2012). IFN Regulatory Factor 8 Is a Key Constitutive Determinant of the Morphological and Molecular Properties of Microglia in the CNS. PLoS ONE, 7. source
The Results section on altered molecular properties reports significantly reduced Iba1 levels in IRF8-deficient microglia. The Results section on phagocytosis reports no significant difference from wild-type microglia in fluorescent E. coli particle uptake across the tested time points, supporting the stated absence of a detected phagocytosis deficit in that assay. (LLM, conf=0.93)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“As a lysosomal marker, CD68 is mainly expressed in the soma of ramified microglia. Therefore, the typical extrusions cannot not be observed with CD68 staining ([27], Figure 1), making it a non-suitable marker in the examination of microglial morphology.”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 7. CD68
What the sources say
- Supportedcites [27] Hendrickx, 2017, Staining of HLA-DR, Iba1 and CD68 in human microglia reveals partially overlapping expression depending on cellular morphology and pathology, J. Neuroimmunol. source
The passage labeled “Nimmerjahn” says CD68 is primarily on lysosomal membranes, that lysosomes in ramified microglia are mainly near the nucleus, and that typical extrusions therefore cannot be observed with CD68 staining. The conclusion says CD68 is least useful for studying morphology because of its intracellular expression. Page numbers are not provided in our copy. (LLM, conf=0.94)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, subsequent downregulation of P2RY12 induces the retraction of microglial processes and therefore leads to morphological activation [57].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 4. P2RY12
What the sources say
- Partly supportedcites [57] Koizumi, 2013, Purinergic receptors in microglia: Functional modal shifts of microglia mediated by P2 and P1 receptors, Glia sourceExperimental — accuracy not yet measured
The PROCESS-RETRACTING MICROGLIA section (page not provided) reports that LPS activation decreases P2Y12 expression and that a change in the balance of P2Y12 and A2A receptors may partly explain a shift toward amoeboid morphology. It attributes process retraction to adenosine signaling through A2A, not to P2Y12 downregulation alone. The claim therefore overstates a causal role for P2Y12 downregulation. (LLM, conf=0.87)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“CD74 is also known as the invariant chain and it is necessary for blocking the peptide-binding site of MHCII molecules during their transport from the endoplasmatic reticulum to the cell surface [66,67,68].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 5. CD74
What the sources say
- Partly supportedcites [66] Radomir, 2017, CD74 is a novel transcription regulator, Proc. Natl. Acad. Sci. USA sourceExperimental — accuracy not yet measured
The opening section (page unavailable) says CD74 functions as an MHC class II chaperone, and the References identify invariant chain with CD74. Our copy does not say that CD74 blocks the MHCII peptide-binding site or specify that it does so during transport from the endoplasmic reticulum to the cell surface. (LLM, conf=0.84)
- Supportedcites [67] 2016, The multifaceted roles of the invariant chain CD74—More than just a chaperone, Biochim. Biophys. Acta Bioenerg. source
Section 3 states that CD74 blocks the MHCII antigen-binding site and prevents premature peptide binding during the biosynthetic pathway. Sections 3 and 3.1 describe its association with MHCII in the ER and its role in directing MHCII to antigen-processing compartments, supporting the transport context of the paraphrase. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [68] Arie, 2005, CD74 Is a Member of the Regulated Intramembrane Pro-teolysis-processed Protein Family, Mol. Biol. Cell source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Furthermore, MHCII expression precedes and regulates dopaminergic neurodegeneration in the substantia nigra [94,95,96].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 6. MHCII
What the sources say
- Not checked — no full text of the sourcecites [94] Jewett, 2021, The MHC class II transactivator modulates seeded alpha-synuclein pathology and dopaminergic neurodegeneration in an in vivo rat model of Parkinson’s disease, Brain Behav. Immun. source
- Partly supportedcites [95] Subbarayan, 2020, T cell infiltration and upregulation of MHCII in microglia leads to accelerated neuronal loss in an α-synuclein rat model of Parkinson’s disease, J. Neuroinflamm. sourceExperimental — accuracy not yet measured
The Results section (Fig. 6; page not provided) says microglial MHCII expression increased alongside dopamine-neuron loss in the substantia nigra, not that it preceded the loss. The Discussion says the findings suggest that T-cell interaction with microglia involving MHCII upregulation is necessary for neuronal loss in this α-synuclein rat model, supporting a qualified regulatory role. (LLM, conf=0.87)
- Supportedcites [96] Harms, 2013, MHCII is required for α-synuclein-induced activation of microglia, CD4 T cell proliferation, and dopaminergic neurodegeneration, J. Neurosci. source
In the α-synuclein overexpression mouse model, the Results report increased microglial MHCII expression in the substantia nigra at 4 weeks and dopaminergic neuron loss at 6 months. The same section reports that MHCII knockout prevented that neuron loss, supporting a regulatory role in this model. (LLM, conf=0.90)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“In an analysis of 16,096 individual microglial transcriptomes, the cluster depicting a distinct upregulation of CD68 was most enriched for DAM genes, such as CD74, HL-DRB1 and ITM2B and was associated with pathologic conditions, such as inflammatory demyelination, ischemia and AD [39].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 7. CD68
What the sources say
- Partly supportedcites [39] Olah, 2020, Single cell RNA sequencing of human microglia uncovers a subset associated with Alzheimer’s disease, Nat. Commun. sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Tests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“Since, in this study, microglia that were positive for P2RY12 also expressed markers of activation, such as CD68, progranulin and to a limited extent, HLA-DR, the mere homeostatic function of P2RY12 needs to be challenged.”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 4. P2RY12
What the sources say
- Supportedcites [64] Walker, D.G., Tang, T.M., Mendsaikhan, A., Tooyama, I., Serrano, G.E., Sue, L.I., Beach, T.G., and Lue, L.-F. (2020). Patterns of Expression of Purinergic Receptor P2RY12, a Putative Marker for Non-Activated Microglia, in Aged and Alzheimer’s Disease Brains. Int. J. Mol. Sci., 21. source
The Introduction reports CD68 and progranulin in most P2RY12-positive microglia and says that classifying P2RY12 expression as a marker of homeostatic microglia needs reconsideration. Results §2.6 reports limited colocalization with HLA-DR, matching the claim’s qualification. (LLM, conf=0.92)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“It is indicative of phagocytic activity [2], and is upregulated in cell culture experiments after treatment with pro-inflammatory cytokines, lipopolysaccharide (LPS) and IFNγ [98].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 7. CD68
What the sources say
- Supportedcites [2] Walker, 2015, Immune phenotypes of microglia in human neurodegenerative disease: Challenges to detecting mi-croglial polarization in human brains, Alzheimers Res. Ther. source
The CD68 section states that CD68 is upregulated in actively phagocytic cells, supporting the clause attributed to this source [2]. The cell-culture treatment clause is separately attributed to [98] and is not part of this verdict. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites [98] Wong, 2005, Macrosialin increases during normal brain aging are attenuated by caloric restriction, Neurosci. Lett. source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“TMEM119 has been shown to be stably and specifically expressed in microglia [41,44], and it can be used to distinguish microglia from resident and infiltrating macrophages [41].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 3. TMEM119
What the sources say
- Supportedcites [41] Bennett, 2016, New tools for studying microglia in the mouse and human CNS, Proc. Natl. Acad. Sci. USA source
The section “Tmem119 Is a Specific and Stable Marker of Microglia in Mouse and Human” describes it as highly specific and reports stable identification after injury and inflammation. “Macrophages After CNS Inflammation and Injury” reports that Tmem119 labeled resident microglia, not infiltrating macrophages; the mRNA-specificity section also reports its absence from meningeal, choroid plexus, and perivascular macrophages. (LLM, conf=0.94)
- Partly supportedcites [44] Bonham, 2019, The Transcriptional Landscape of Microglial Genes in Aging and Neurodegenerative Disease, Front. Immunol. sourceExperimental — accuracy not yet measured
The Introduction describes TMEM119 as a specific microglial marker that distinguishes microglia from other myeloid cells, including perivascular and infiltrating macrophages. The Methods also calls it a highly specific, well-validated marker. Neither passage establishes that its expression is stable, so that part of the claim is unsupported. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Supported
In the paper
“Formerly thought to be expressed by all microglial subpopulations [2], our group identified areas in the human hippocampus where a localized loss of IBA1 expression was observed [21], whereas other microglial markers, such as GPX1 or P2RY12, were still present.”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Not checked — no full text of the sourcecites [21] Lier, 2019, Loss of IBA1-Expression in brains from individuals with obesity and hepatic dysfunction, Brain Res. source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Morphologically, the following four microglial phenotypes can be distinguished: resting, activated, amoeboid, and dystrophic microglia (Table 1, Figure 1).”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 1. Introduction
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
In the paper
“Since its first description in 1998 [3], IBA1 has been the most widely used marker for the immunohistochemical analysis of microglia.”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 2. IBA1
What the sources say
- Not checked — no full text of the sourcecites [3] Ito, 1998, Microglia-specific localisation of a novel calcium binding protein, Iba1, Mol. Brain Res. source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“However, it was shown that CD74 expression occurred independently from concomitant MHCII expression, and it is also expressed on non-antigen-presenting cells [69].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 5. CD74
What the sources say
- Not checked — no full text of the sourcecites [69] Henne, 1995, Surface expression of the invariant chain (CD74) is independent of concomitant expression of major histocompatibility complex class II antigens, Immunology
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“The G-protein-coupled purinergic receptor P2RY12 [51] is specific for parenchymal microglia [52] and shows a persistent expression during the lifespan of microglia [53].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 4. P2RY12
What the sources say
- Not checked — no full text of the sourcecites [52] 2021, Shaping Neuronal Fate: Functional Heterogeneity of Direct Microglia-Neuron Interactions, Neuron source
- Not checked — no full text of the sourcecites [53] Mildner, 2017, P2Y12receptor is expressed on human microglia under physiological conditions throughout development and is sensitive to neuroinflammatory diseases, Glia source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“However, necrotic lesions of cerebral infarctions and demyelinating lesions of multiple sclerosis were devoid of TMEM119 expression [45].”
§ Beyond Activation: Characterizing Microglial Functional Phenotypes > 3. TMEM119
What the sources say
- Not checked — no full text of the sourcecites [45] Satoh, 2016, TMEM119 marks a subset of microglia in the human brain, Neuropathology source
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
Microglia are not replenished by blood-borne mononuclear cells under physiological circumstances.
“Since microglia are not replenished by blood-borne mononuclear cells under physiological circumstances”
The authors state this as an assumption.
Certain microglial dysfunctions associated with a loss of IBA1 may not be pathology specific, but have a broader impact on immune defense and synaptic plasticity.
“it is reasonable to assume that certain microglial dysfunctions that are associated with a loss of IBA1 may not be pathology specific, but have a broader impact on their role in immune defense and synaptic plasticity.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“Moreover, decreased Iba1 expression and even Iba1- microglia have previously been described in neurodegenerative disorders such as Huntington’s and Alzheimer’s disease50.”
From CHIT1 at diagnosis predicts faster disability progression and reflects early microglial activation in multiple sclerosis (2024) · cites this paper as [50]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Huntington's disease claim cites an Alzheimer's disease paper
MinorThe text attributes a finding about Huntington's disease to Bulk et al. [25], but the listed title of reference 25 identifies its subject as early- and late-onset Alzheimer's disease.
“In the striatum, Bulk et al. [25] demonstrated an association between an advanced disease state in patients suffering from Huntington’s disease and IBA1-negative microglia.”
“Bulk M. Abdelmoula W.M. Nabuurs R.J.A. van der Graaf L.M. Mulders C.W.H. Mulder A.A. Postmortem MRI and histology demonstrate differential iron accumulation and cortical myelin organization in early- and late-onset Alzheimer’s disease”
Citations
Cites
A Unique Microglia Type Associated with Restricting Development of Alzheimer’s Disease
Keren-Shaul, H., Spinrad, A., Weiner, A., Matcovitch-Natan, O., Dvir-Szternfeld, R., Ulland, T. K., David, E., Baruch, K., Lara-Astaiso, D., Toth, B., et al. (2017) · Cell · doi:10.1016/j.cell.2017.05.018 · Cited by 5,493 · cited 4×
“[28] demonstrated significant changes in the rodent gene expression of disease-associated microglia (DAM), a concept that was primarily described in a mouse model of Alzheimer’s disease [28].”
BackgroundInfluentialKrasemann, S., Madore, C., Cialic, R., Baufeld, C., Calcagno, N., El Fatimy, R., Beckers, L., O’Loughlin, E., Xu, Y., Fanek, Z., et al. (2017) · Immunity · doi:10.1016/j.immuni.2017.08.008 · Cited by 2,979
Variant of TREM2 Associated with the Risk of Alzheimer's Disease
Jonsson, T., Stefansson, H., Steinberg, S., Jonsdottir, I., Jonsson, P. V., Snaedal, J., Bjornsson, S., Huttenlocher, J., Levey, A. I., Lah, J. J., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1211103 · Cited by 2,558 · cited 1×
“The triggering receptor expressed on myeloid cells (TREM)-2 serves as a binding partner for apolipoprotein E (APOE, [29]), and especially the ε4 allele has been shown to act as a risk factor for Alzheimer’s disease [30,31].”
BackgroundIdentification of a unique TGF-β–dependent molecular and functional signature in microglia
Butovsky, O., Jedrychowski, M. P., Moore, C. S., Cialic, R., Lanser, A. J., Gabriely, G., Koeglsperger, T., Dake, B., Wu, P. M., Doykan, C. E., et al. (2014) · Nature Neuroscience · doi:10.1038/nn.3599 · Cited by 2,543
Hammond, T. R., Dufort, C., Dissing-Olesen, L., Giera, S., Young, A., Wysoker, A., Walker, A. J., Segel, M., Nemesh, J., Saunders, A., et al. (2018) · doi:10.1101/406140 · Cited by 2,225
Heterogeneity in the distribution and morphology of microglia in the normal adult mouse brain
Lawson, L. J., Perry, V. H., Dri, P., & Gordon, S. (1990) · Neuroscience · doi:10.1016/0306-4522(90)90229-w · Cited by 2,045 · cited 1×
“While the distribution of microglia varies between different brain regions [11], the expression of allograft inflammatory factor 1 (AIF-1, gene for IBA1) on microglia does not differ between white matter and grey matter [12].”
BackgroundObesity is associated with hypothalamic injury in rodents and humans.
Thaler, J. P., Yi, C.-X., Schur, E. A., Guyenet, S. J., Hwang, B. H., Dietrich, M. O., Zhao, X., Sarruf, D. A., Izgur, V., Maravilla, K. R., et al. (2012) · Journal of Clinical Investigation · doi:10.1172/jci59660 · Cited by 1,857
New tools for studying microglia in the mouse and human CNS
Bennett, M. L., Bennett, F. C., Liddelow, S. A., Ajami, B., Zamanian, J. L., Fernhoff, N. B., Mulinyawe, S. B., Bohlen, C. J., Adil, A., Tucker, A., et al. (2016) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1525528113 · Cited by 1,804 · cited 2×
“In human brains, at least 50% of the IBA1-positive microglial population were positive for TMEM119 [45], while rodent studies even demonstrated an expression of 98% of CD45lowCD11b+ cells in adult animals [41].”
BackgroundA polarizing question: do M1 and M2 microglia exist?
Ransohoff, R. M. (2016) · Nature Neuroscience · doi:10.1038/nn.4338 · Cited by 1,573
The P2Y12 receptor regulates microglial activation by extracellular nucleotides
Haynes, S. E., Hollopeter, G., Yang, G., Kurpius, D., Dailey, M. E., Gan, W.-B., & Julius, D. (2006) · Nature Neuroscience · doi:10.1038/nn1805 · Cited by 1,542
Flagged first, then by citations
2 of the 112 references couldn’t be matched to a known paper.
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Items 101–200 of 278
A simple protocol for isolating microglia from adult mouse brain
Chakrabarti, S., Gorai, S., & Pahan, K. (2023) · NeuroImmune Pharmacology and Therapeutics · doi:10.1515/nipt-2023-0014 · Cited by 7
Oxysterol Induces Expression of 60 kDa Chaperone Protein on Cell Surface of Microglia
Kim, K., Cho, H.-R., Kim, B.-Y., Kim, J., Park, D., Kwon, R. J., & Son, Y. (2024) · International Journal of Molecular Sciences · doi:10.3390/ijms25169073 · Cited by 7
Targeting Spermine Oxidase to Mitigate Traumatic Brain Injury Pathology in the Aging Brain
Sun, J., Jan, J., Yen, T., Chen, Y., Teng, R.-D., Yang, C., & Hsieh, C. T. (2025) · Antioxidants · doi:10.3390/antiox14060709 · Cited by 7
“Following CCI, we observed a pronounced morphological shift in microglial cells from a resting, ramified state to an activated, amoeboid morphology, indicative of profound microgliosis [37,38].”
Tarhan, S. Z., Pepe, N. A., Şen, A., & İşoğlu, İ. A. (2025) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2025.145837 · Cited by 9
Russo, M., Pellegrino, G., Faure, H., Tirou, L., Sharif, A., & Ruat, M. (2024) · Brain Structure and Function · doi:10.1007/s00429-023-02756-2 · Cited by 7
“4C), in agreement with the distribution of IBA1-positive microglial cells (Lier et al. 2021).”
ResultMelkumyan, M., Annaswamy, V. M., Evans, A. M., Showemimo, O., McCullers, Z., Sun, D., Murphy, T. E., Vrana, K. E., Arnold, A. C., Raup‐Konsavage, W. M., et al. (2024) · Frontiers in Neuroscience · doi:10.3389/fnins.2024.1375440 · Cited by 7
“We next stained CeA sections for Iba1, a microglial-specific marker that allows for analysis of overall cell numbers, as well as microglia morphology to assess activation states (Lier et al., 2021; Coker et al., 2022).”
MethodELK4 ameliorates cognitive impairment and neuroinflammation induced by obstructive sleep apnea
Yang, H., Yuan, Y., Ke, Y., Wang, N., & Li, X. (2024) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2024.111054 · Cited by 7
“Since its first description in 1998, Iba1 has been the most widely used marker for the immunohistochemical analysis of microglia, and Iba1 reliably stains ramified, activated, amoeboid, and dystrophic microglia (Lier et al., 2021).”
An, Y., Su, G., Chen, W., Song, J., Chai, M., Zhu, L., & Zhang, Z. (2025) · Neurochemistry International · doi:10.1016/j.neuint.2025.105949 · Cited by 7
Holtman, I. R., Glass, C. K., & Nott, A. (2024) · Advances in neurobiology · doi:10.1007/978-3-031-55529-9_29 · Cited by 6
Restoring neuropetide Y levels in the hypothalamus ameliorates premature aging phenotype in mice
Ferreira‐Marques, M., Carmo‐Silva, S., Pereira, J. A., Botelho, M., Nóbrega, C., López-Otín, C., de Almeida, L. P., Aveleira, C. A., & Cavadas, C. (2025) · GeroScience · doi:10.1007/s11357-025-01574-0 · Cited by 7
“The decreased Iba1 may reflect either reduced activation or a loss of microglial cells, which can have significant implications for immune surveillance and neural homeostasis [73, 74].”
Feng, Y., Wei, Z., Li, R. P., Shi, Q., & Jinyan, C. (2025) · Journal of Ethnopharmacology · doi:10.1016/j.jep.2025.120695 · Cited by 8
Zhu, D., Wang, M., Liu, F., Zhan, S., Feng, Y., Li, C., Yi, Y., Li, C., Zhou, C., Zhang, Y., et al. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.106128 · Cited by 7
Ortega, A. J., Daniel, S., Renwick, M., Kambhampati, P., Thompson, K. N., Collier, G. E., Baker, E. L., Zaki, H., & Hulleman, J. D. (2025) · Cell Death and Disease · doi:10.1038/s41419-025-08104-y · Cited by 7
“C), re fl ecting an activated state [98, 99].”
Preszler, C., Stieger, K. C., Chen, K., Zhang, G., & Kozai, T. D. Y. (2026) · Journal of Neural Engineering · doi:10.1088/1741-2552/ae4652 · Cited by 8
“Microglial morphology provides a direct readout of activation state, with homeostatic microglia exhibiting highly ramified processes and activated microglia adopting a less branched, amoeboid morphology [15, 26, 68].”
Martín-López, E., Brennan, B., Mao, T., Spence, N. J., Meller, S. J., Han, K., Yahiaoui, N., Wang, C., Iwasaki, A., & Greer, C. A. (2024) · eNeuro · doi:10.1523/eneuro.0106-24.2024 · Cited by 6
“…identi fi ed by small round cell bodies that extend highly branched thin processes (rami fi ed microglia), and activated microglia, whose morphology become amoeboid and hypertrophic, characterized by large cell bodies with shorter thicker processes (Blackbeard et al., 2007; Lier et al., 2021).”
BackgroundUSP22 inhibits microglial M1 polarization by regulating the PU.1/NLRP3 inflammasome pathway
Yu, M., Li, X., Ning, M.-L., Yan, Z.-Z., & Yu, W.-T. (2024) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2024.111157 · Cited by 6
Xie, Y., Qin, Y., Wang, J., Xu, Z., Chen, L., Kuang, Y., Yang, R., & Huang, L. (2025) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-025-03828-2 · Cited by 6
“Atrophic microglia have lost branches, and their cell bodies may be swollen or thin, often indicating functional loss, and are commonly found in the brains of patients with AD (Lier et al. 2021).”
Zhang, Z., Wang, X., Lin, Y., & Pan, D. (2022) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2022.944883 · Cited by 7
“In this study, we first aim to develop a versatile tool by taking advantage of Transmembrane protein 119 (Tmem119), a recently identified homeostatic marker specific for resident microglia (Lier et al., 2021), to quantify microglia proliferation and activation independently.”
BackgroundMethodCatalano, F., Vlaar, E. C., Katsavelis, D., Dammou, Z., Huizer, T. F., van den Bosch, J. C., Hoogeveen‐Westerveld, M., van den Hout, J. M. P., Oussoren, E., Ruijter, G. J. G., et al. (2023) · Molecular Therapy — Methods & Clinical Development · doi:10.1016/j.omtm.2023.101149 · Cited by 6
“33,34 We observed a widespread increase of CD68 immunoreactivity in brains of Ids y/ (cid”
BackgroundWeathered, C., Bardehle, S., Yoon, C., Kumar, N. N., Leyns, C. E. G., Kennedy, M. E., Bloomingdale, P., & Pienaar, E. (2023) · CPT Pharmacometrics & Systems Pharmacology · doi:10.1002/psp4.13095 · Cited by 6
“23 Once activated, microglia cannot return to an inactive state or anti-inflammatory state during the simulation.”
BackgroundWakid, M. H., Alsulami, M. N., Farid, M., & Kholy, W. A. E. (2023) · Infection and Drug Resistance · doi:10.2147/idr.s443047 · Cited by 9
“11,12 Also, Ide et al (2011) 13 found that normal epidermal LCs and dermal histiocytes also express Iba1.”
BackgroundSpinal cord microglia drive sex differences in ethanol-mediated PGE2-induced allodynia
Alexander, S. N., Reed, O. A., & Burton, M. D. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.08.026 · Cited by 6
“CD206) markers (Jurga et al., 2020; Lier et al., 2021; Paolicelli et al., 2022).”
Bar, E., Fischer, I., Rokach, M., Elad‐Sfadia, G., Shirenova, S. D., Ophir, O., Trangle, S. S., Okun, E., & Barak, B. (2024) · Glia · doi:10.1002/glia.24519 · Cited by 5
Microglial galectin-3 increases with aging in the mouse hippocampus
Shin, H. J., Lee, S. J., An, H. S., Choi, H. N., Jeong, E. A., Lee, J. W., Kim, K. E., Choi, B.-H., Yun, S. P., Kang, D., et al. (2025) · Korean Journal of Physiology and Pharmacology · doi:10.4196/kjpp.24.196 · Cited by 7
“196 immune cells in the brain, which play a protective role in defending the brain from damage [10,11].”
Obst, S., Serdar, M., Herz, J., Kempe, K., Assili, M., Rizazad, M., Hirani, D., Alcazar, M. A. A., Endesfelder, S., Möbius, M. A., et al. (2025) · Cells · doi:10.3390/cells14060443 · Cited by 7
“Furthermore, CD68 is only one single marker, which might not solely characterise activated and pro-inflammatory microglia [64].”
Zou, Y., Jiang, J., Li, Y., Ding, X., Tong, Q., Shi, Y., Xiao, L., & Chen, L. (2025) · Advanced Science · doi:10.1002/advs.202400747 · Cited by 6
Brain region and sex differences in human microglia morphology and function
Yoblinski, A. R., Dubey, J., Myers, T., Sathees, N., Volk, D. W., Fish, K. N., & Seney, M. L. (2025) · Cerebral Cortex · doi:10.1093/cercor/bhaf120 · Cited by 6
The role of liver macrophages in viral liver pathogenesis
Brantly, A., Yeakle, K., Bouchard, M. J., Gaskill, P. J., & Nonnemacher, M. R. (2025) · Journal of Leukocyte Biology · doi:10.1093/jleuko/qiaf088 · Cited by 7
Lisi, L., Olivi, A., Ciotti, G. M. P., Marino, S., Ferraro, C., Menna, G., Martire, M., Pennisi, G., Navarra, P., & Pepa, G. M. D. (2024) · Neurochemistry International · doi:10.1016/j.neuint.2024.105922 · Cited by 5
Development of cerebral microhemorrhages in a mouse model of hypertension
Xie, D. F., Fang, C., Crouzet, C., Hung, Y.-H., Vallejo, A., Lee, D., Liu, J., Liu, H., Muvvala, S., Paganini‐Hill, A., et al. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03378-7 · Cited by 8
The effects of urolithin A on poly I:C-induced microglial activation
Mingo, Y. B., Gabele, L., Lonnemann, N., Brône, B., Körte, M., & Hosseini, S. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1343562 · Cited by 5
“For this purpose, immunostaining was performed for IBA-1 and CD68, which are known to be upregulated in reactive microglial cells (Lier et al., 2021).”
MethodSong, S., Druschel, L. N., Kasthuri, N. M., Wang, J., Conard, J. H., Chan, E. R., Acharya, A. P., & Capadona, J. R. (2024) · Scientific Reports · doi:10.1038/s41598-024-68017-2 · Cited by 6
“Upon activation, TMEM119 concentrations are reduced in microglia 56 .”
BackgroundClain, J., Couret, D., Bringart, M., Meilhac, O., d’Hellencourt, C. L., & Diotel, N. (2024) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2024.12.002 · Cited by 6
Vasanthi, S. S., Massey, N., Meyer, C., Wang, C., & Thippeswamy, T. (2025) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2025.118234 · Cited by 4
“Phagocytic or reactive microglia more commonly contain CD68 therefore, we further co-stained IBA1 with CD68 to determine whether co-labeled cells were affected by DFP and SAR treatments [55,56].”
Okano, Y., Kase, Y., & Okano, H. (2022) · Stem Cell Reports · doi:10.1016/j.stemcr.2022.10.015 · Cited by 6
TAMing Gliomas: Unraveling the Roles of Iba1 and CD163 in Glioblastoma
Fuse, H., Zheng, Y., Alzoubi, I., & Graeber, M. B. (2025) · Cancers · doi:10.3390/cancers17091457 · Cited by 7
“However, our results align with other studies [63–65] that demonstrate a significant increase in Iba1 expression in microglia responding to glioma.”
Research progress on platelet factor 4 in improving cognition
Zhuo, H., Chen, N., Hu, X., & Liu, Z. (2025) · Experimental Neurology · doi:10.1016/j.expneurol.2025.115403 · Cited by 4
Digby, Z., Diamond, C., Wescott, H., Smolak, P. J., Thornton, P., Lindsay, N. A., Gabel, C. A., Clarke, N. P., & Watt, A. P. (2026) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.5c00843 · Cited by 4
Viil, J., Somelar, K., Jaako, K., Anier, K., & Zharkovsky, A. (2022) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-022-01285-6 · Cited by 7
Yassine, M., Hassan, S. A., Yücel, L. A., Purath, F. F. A., Korf, H., von Gall, C., & Ali, A. A. H. (2024) · Biomedicines · doi:10.3390/biomedicines12102202 · Cited by 4
“We analyzed whether HCC induced microglial activation in SCN as an in fl amma-tory response by use of IBA-1, the most commonly used marker for microglia [48].”
MethodDetection of molecular markers of ferroptosis in human Alzheimer's disease brains
Mayr, E., Rotter, J., Kuhrt, H., Winter, K., Stassart, R. M., Streit, W. J., & Bechmann, I. (2024) · Journal of Alzheimer s Disease · doi:10.1177/13872877241296563 · Cited by 9
“4,48,49 We detected the area of all ferritin-positive microglia relative to the total area of the evaluated section (ferritin area ratio in %).”
Self-citationMaya-Arteaga, J. P., Martínez-Orozco, H., & Díaz-Cintra, S. Y. (2024) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1505048 · Cited by 6
Yun, J. (2025) · Frontiers in Endocrinology · doi:10.3389/fendo.2025.1609796 · Cited by 4
Gou, L., Zheng, H., Chen, J., Gao, Y., Ma, J., Chen, D., Li, Z., Wu, C., Lian, B., Zhang, X., et al. (2025) · Molecular Psychiatry · doi:10.1038/s41380-025-03171-1 · Cited by 5
Sexually differentiated microglia and CA1 hippocampal synaptic connectivity
Prengel, T. M., Brunne, B., Habiballa, M., & Rune, G. M. (2023) · Journal of Neuroendocrinology · doi:10.1111/jne.13276 · Cited by 4
Tran, N. T., Penny, T. R., Chan, K. Y. Y., Tang, T., Papagianis, P. C., Sepehrizadeh, T., Nekkanti, L. P., Zahra, V. A., Pham, Y., Yawno, T., et al. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03053-3 · Cited by 4
“Morphological assessment delineates whether microglia are in a resting (ramified) or activated (ame-boid) state [36] (Fig.”
BackgroundChéry, S. L., O’Buckley, T. K., Boero, G., Balan, I. S., & Morrow, A. L. (2024) · Alcoholism Clinical and Experimental Research · doi:10.1111/acer.15404 · Cited by 4
From Organotypic Mouse Brain Slices to Human Alzheimer Plasma Biomarkers: A Focus on Microglia
Steiner, K., Yılmaz, N., Gern, A., Marksteiner, J., Faserl, K., Villunger, M., Sarg, B., & Humpel, C. (2024) · Biomolecules · doi:10.3390/biom14091109 · Cited by 6
“Additionally, we verified successful human plasma printing by visualizing MCP-1 spiked into the plasma samples.”
MethodQuintanilla, M. E., Morales, P., Santapau, D., Gallardo, J., Rebolledo, R., Riveras, G., Acuña, T., Herrera‐Marschitz, M., Israel, Y., & Ezquer, F. E. (2024) · PLoS ONE · doi:10.1371/journal.pone.0312828 · Cited by 5
Arnanz, M. A., Ferrer, M., Grande, M. T., Esteban, S. R. D. M., Ruiz‐Pérez, G., Cravatt, B. F., Mostany, R., Lobo, V. J. S.-A., Romero, J., & Martínez-Relimpio, A. M. (2024) · Glia · doi:10.1002/glia.24638 · Cited by 4
“We also analyzed microglial morphology due to its close relation to cellular function (Lier et al., 2021).”
Arcella, A., Alborghetti, M., Traficante, A., et al. (2024) · Current Neuropharmacology · doi:10.2174/1570159x23666241209090326 · Cited by 4
“The expression of the ionized calcium-binding adapter molecule 1 (IBA1), which is up-regulated in activated macrophages and microglia, was also evaluated [21].”
Godeanu, S., Mușat, M. I., Scheller, A., Osiac, E., & Cătălin, B. (2025) · Frontiers in Neuroanatomy · doi:10.3389/fnana.2024.1507140 · Cited by 4
Kelemen, K., Sárosi, M., Csüdör, Á., Orbán-Kis, K., Kelemen, H., Bába, L., Gáll, Z., Horváth, E., Katona, I., & Szilágyi, T. (2025) · Frontiers in Pharmacology · doi:10.3389/fphar.2025.1553545 · Cited by 5
Yang, X., Li, Y., & Wei, Z. (2025) · MethodsX · doi:10.1016/j.mex.2025.103306 · Cited by 4
“Iba1 is a widely used marker for visualizing microglial morphology and distribution in the brain [ 10 ], while CD68 is a lysosomal marker associated with phagocytic activity and commonly used to assess activated microglia [ 11 ].”
Shen, Y., Cui, J., Zhang, S., Wang, Y., Wang, J., Su, Y., Xu, D., Liu, Y., Guo, Y., & Bai, W. (2022) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2022.956342 · Cited by 4
“We concentrated on temporal morphological changes, but more comprehensive research using various qualitative and quantitative techniques would be needed to address the topic of the neurovascular unit, including the temporal alteration of different functional microglial phenotypes (Lier et al., 2021), how other compone…”
BackgroundEvaluation of the Effect of β-Wrapin AS69 in a Mouse Model Based on Alpha-Synuclein Overexpression
Höfs, L., Geißler-Lösch, D., Wunderlich, K., Szegő, É. M., den Haute, C. V., Baekelandt, V., Hoyer, W., & Falkenburger, B. H. (2024) · Biomolecules · doi:10.3390/biom14070756 · Cited by 3
“Furthermore, amoeboid and rod-shaped microglial cells are associated with phagocytic activity and antigen representation [15].”
BackgroundMethodMicroglia express Tie2 in a longitudinal imaging study of acute neural injury in mice
Brodsky, J., Tashi, Z., Christopher, K. S., Kruitoff, R., Abbasi, M. A., Cerna, G., Gohsman, S. B., Mana, M., & Bartelle, B. B. (2025) · Molecular Biology of the Cell · doi:10.1091/mbc.e25-05-0257 · Cited by 4
“(Figure 4, B and D), with little pixelwise correlation ( r = 0.17) (Lier et al. , 2021).”
InfluentialHarnessing the innate immune system for glioblastoma therapeutics
McLean, H., Drill, M., Sequeira, R. P., Jayakrishnan, P. C., Jeffree, R. L., Hunn, M., O'Brien, T. J., Hamilton, J., & Monif, M. (2025) · Journal of Neuroimmunology · doi:10.1016/j.jneuroim.2025.578713 · Cited by 3
“In contrast, activated microglia have a larger cell body, with the presence of lamellipodia (Lier et al., 2021; Vidal-Itriago et al., 2022).”
Cerebellar dysfunction in a mouse model of childhood-onset manganese-induced dystonia parkinsonism
Rodichkin, A. N., Brown, A. M., Devabathini, P., McGlothan, J. L., Chen, S., Pattammattel, A., Chu, Y. S., Lin, T., Pontow, D. D., Abilmouna, K., et al. (2025) · Neurobiology of Disease · doi:10.1016/j.nbd.2025.107115 · Cited by 3
Abnormal behaviors and glial responses in an animal model of tau pathology
Liu, Y., Sobue, A., Sahara, N., Isobe, M., Tanaka, R., Zhu, Y., Zhu, W., Matsuzaki, T., Yamanaka, K., Yamada, K., et al. (2025) · Molecular Brain · doi:10.1186/s13041-025-01252-4 · Cited by 3
“Our data are consistent with previous reports that markers of DAM, such as Apoe, Trem2, Cst7 , and Axl [31, 32], and those of activated phagocytosis in macrophages and microglia, such as Cd68 and Cd11c [68], are upregulated in rTg4510 mice.”
Seidel, F., Fluiter, K., Kleemann, R., Worms, N., van Nieuwkoop, A., Caspers, M. P. M., Grigoriadis, N., Kiliaan, A. J., Baas, F., Michailidou, I., et al. (2023) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2023.1205261 · Cited by 3
“The increase in CD68-positive microglia suggests that HFD-induced obesity promotes microglia phagocytic activity (Lier et al., 2021).”
BackgroundPrantzalos, E. R., Chesser, J. P., Logan, J. S., McLaurin, K. A., Anderson, C. D., Gabbard, J. D., Severson, W. E., Palmer, K. E., Mullins, B. J., Dwoskin, L. P., et al. (2025) · Scientific Reports · doi:10.1038/s41598-025-00738-4 · Cited by 3
“…visual inspection of the IBA1 staining, COVID-19 negative groups appeared to exhibit a more ramified microglial morphological phenotype, while the COVID-19 positive groups display a more activated phenotypical appearance evidenced by the shortened ramifications and increased size of cell soma 57 .”
InfluentialZeng, F., Tiwari, S., Chok, A., Zhou, Y., Zhao, Y., Chen, X., Hao, Y., Zhu, K., Kettenmann, H., & Xiang, X. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.07.013 · Cited by 4
Plantera, L., Immig, K., Fritsche, A., Reinicke, M., Zemer, A., Monsonego, A., Ceglarek, U., & Bechmann, I. (2025) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.70168 · Cited by 3
“In fact, chronic activation and excessive phagocytosis might cause microglial senescence observed in the aged human brain, which we regard as a form of immune exhaustion [4, 19–23].”
Self-citationSu, P. P., He, L., Zhang, L., Yu, J., & Guan, Z. (2025) · Pain · doi:10.1097/j.pain.0000000000003722 · Cited by 3
Reliable detection of RNA in hippocampus sections of mice by FISH up to a post-mortem delay of 24 h
Seiffer, S., Brendler, J., Schulz, A., & Ricken, A. M. (2024) · Histochemistry and Cell Biology · doi:10.1007/s00418-024-02277-x · Cited by 3
“Changes in the shape and Gpr34/P2ry12 gene expression have been described in the activation of microglia, which occurs in numerous neurodegenerative diseases such as Alzheimer’s disease (Haque et al. 2018; Lier et al. 2021; Schöneberg et al. 2018).”
BackgroundAcute liver damage generates age independent microglia morphology changes in mice
Nedelea, G., Mușat, M. I., Mitran, S. I., Ciorbagiu, M. C., & Cătălin, B. (2025) · Romanian Journal of Morphology and Embryology · doi:10.47162/rjme.65.4.15 · Cited by 3
“The microglia reaction to acute events is well documented in both focal ischemia [10–12] and global hypoxia [13], where significant alterations can occur within just a few minutes up to 10 days, with a progressive reversal of their morphology [14, 15].”
Salia, S., Burke, F. F., Hinks, M., Randell, A. M., Matheson, M. A., Walling, S. G., & Swift‐Gallant, A. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.06.18.599415 · Cited by 3
“The reduction in cell number and microglial processes may in part, reflect an amoeboid phenotype, associated with increased phagocytosis and neuronal death (37).”
BackgroundTsourmas, K. I., Butler, C. A., Kwang, N. E., Sloane, Z. R., Dykman, K. J. G., Maloof, G. O., Prekopa, C. A., Krattli, R. P., El-Khatib, S. M., Swarup, V., et al. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.10.21.619538 · Cited by 4
Novel peptidomimetic compounds attenuate hypoxic-ischemic brain injury in neonatal rats
Chen, X. F., Kroke, B., Ni, J., Munoz, C., Appleman, M., Jacobs, B., Tran, T., Nguyen, K. V., Qiu, C., Stonestreet, B. S., et al. (2025) · Experimental Neurology · doi:10.1016/j.expneurol.2025.115151 · Cited by 2
Microglia-derived sEV: Friend or foe in the pathogenesis of cognitive impairment
Chen, L., & Wang, W. (2025) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2025.111287 · Cited by 3
Almeida, Á. M. A. N., dos Santos, C. C., Takahashi, D., da Silva, L. P., de Sousa, V. M., de Santana, M. R., Arco, A. E. D., dos Santos, B. L., David, J. M., da Silva, V. D. A., et al. (2025) · Molecules · doi:10.3390/molecules30051014 · Cited by 2
“It also promotes debris removal, which contributes to direct inflammation toward its resolution [23].”
Mou, Z., Zheng, Y., Wang, X., Tan, S., Yuan, J., & Li, H. (2025) · Nutritional Neuroscience · doi:10.1080/1028415x.2025.2509337 · Cited by 3
“GFAP, an indicator of gliosis, is typically localized to Müller cells and astrocytes, both of which belong to macroglia cells [38, 39], while Iba-1 labels microglia [40].”
Balderas-Márquez, J. E., Epardo, D., Siqueiros‐Márquez, L., Carranza, M., Luna, M., Quintanar, J. L., Arámburo, C., & Martínez-Moreno, C. G. (2025) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2025.1636399 · Cited by 2
“…instance, M1 state tend to have shorter, less ramified processes, corresponding to their proinflammatory role, whereas M2 microglia exhibit more complex, and highly ramified morphologies, indicative of their tissue repair function (Ramírez et al., 2020; Lier et al., 2021; Fujikawa and Tsuda, 2023).”
Ferri, A., Sacchi, S., Franchi, N., et al. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26189022 · Cited by 2
“As AIF1, also known as Iba-1, is considered a marker of microglial cells in vertebrates [20,46,47], and in the absence of information regarding immune cells associated with neural tissue in P. canaliculata , immunohistochemical staining using Ricinus communis agglutinin 1 (RCA120), which has…”
Gallo, M. T., Golinelli, A., Rizzi, C., Fumagalli, F., Homberg, J. R., Brivio, P., & Calabrese, F. (2025) · Biochemical Pharmacology · doi:10.1016/j.bcp.2025.117632 · Cited by 2
Microglia Polarization: A Key Regulatory Mechanism of Neuropathic Pain
Zhang, T., Liang, W., Gao, J., Liu, H., Li, J., Chen, J., Wang, Y., & Li, J. (2026) · Journal of Pain Research · doi:10.2147/jpr.s557153 · Cited by 2
“15 Microglia can adopt distinct phenotypes according to stimulation, environment and period, which is called microglial polarization.”
Rava, A., Feo, A., Bagnato, G., Doria, V., Pezzullo, M., Petrini, S., Buzzelli, V., Ascone, F., Trapano, M. D., Peruzzi, B., et al. (2026) · Neurobiology of Disease · doi:10.1016/j.nbd.2026.107304 · Cited by 2
Fu, H., Yang, J., & Zhang, M. Y. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1838306 · Cited by 2
“At the molecular phenotype level, mature microglia express specific signature markers including TMEM119 and P2RY12, which are relatively specific to microglia compared to other CNS immune populations (Lier et al., 2021).”
Henao-Restrepo, J. A., Murrieta-Coxca, J. M., Schmeer, C. W., Wei, L., Steiniger, F., Groten, T., Markert, U. R., & Prieto, D. M. M. (2026) · The Journal of Physiology · doi:10.1113/jp289761 · Cited by 4
Microglial reactivity in brainstem chemosensory nuclei in response to hypercapnia
Eugenín, J. L., Beltrán-Castillo, S., Irribarra, E., Pulgar‐Sepúlveda, R., Abarca, N., & Rommy von Bernhardi, M. (2024) · Frontiers in Physiology · doi:10.3389/fphys.2024.1332355 · Cited by 3
“…by small somata, and very thin, long, and arborized branches, become reactive microglia, which show enlarged somata and reduced number and length of branches with scarce arborization (Crain et al., 2013; Doorn et al., 2014; Wolf et al., 2017; Lier et al., 2021; Paolicelli et al., 2022).”
BackgroundRogerson‐Wood, L., Goldsbury, C. S., Sawatari, A., & Leamey, C. A. (2024) · Glia · doi:10.1002/glia.24522 · Cited by 2
“…KO mice, we assayed CD68-labeling in the dLGN at five developmental timepoints — P15, P18, P21, P25, and P30 — in both SE and EE (from birth) cohorts of Ten-m3 KO mice: P15 CD68, a transmembrane lysosomal glycoprotein, is a marker for microglial reactivity (Lier et al., 2021; Schafer et al., 2012).”
BackgroundMethodInfluentialUnraveling the enigma: housekeeping gene Ugt1a7c as a universal biomarker for microglia
Kim, W., Kim, M.-J., & Kim, B. (2024) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2024.1364201 · Cited by 3
“A single microglia biomarker was not suf fi cient to identify them and track their ontogeny and characteristics, especially when there was an interaction with other types of glia/neurons and a transition of status (13, 91 – 93).”
BackgroundHöfling, C., Donkersloot, P., Ulrich, L., Burghardt, S., Opitz, M., Geißler, S., Schilling, S., Cynis, H., Michalski, D., & Roßner, S. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106671 · Cited by 3
“Of note, these cell surface markers are not specific for microglial cells but might be expressed, depending on the experimental setup, also by monocytes and/or infiltrating macrophages (Spiteri et al., 2020; Lier et al., 2021; Vankrie-kelsvenne et al., 2022).”
BackgroundMorphology of Cortical Microglia in the Hyperacute Phase of Subarachnoid Hemorrhage
Lyubomudrov, M. A., Babkina, A. S., Цоколаева, З. И., Yadgarov, M. Y., Shigeev, S. V., Sundukov, D. V., & Golubev, A. M. (2024) · Biology · doi:10.3390/biology13110917 · Cited by 2
“Microglia are known to be very plastic and change their phenotype depending on the microenvironment [43–47].”
Pauletti, A., Gurlo, P., Weiß, E., DePaula-Silva, A. B., Wilcox, K. S., & Bröer, S. (2025) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2024.1528918 · Cited by 2
A Clinically Relevant Mouse Model of Concussion Incorporating High Rotational Forces
Teasell, E. M., Potts, E., Geremia, N. M., Lu, L., Xu, X., Mao, H., & Brown, A. M. (2025) · Neurotrauma Reports · doi:10.1089/neur.2024.0165 · Cited by 2
“22 By contrast, the Iba1-positive microglia in sham mice were highly rami-fi ed and reminiscent of quiescent microglia (inset Fig.”
Badell‐Grau, R. A., Pakravesh, K., Thai, K. E., Son, F., Chen, R., Rainaldi, J., Duong, K., Losay, P., Sivakumar, A., Khare, V., et al. (2025) · Cell Transplantation · doi:10.1177/09636897251323966 · Cited by 2
“We also explored tissue inflammation by examining CD68 expression which is associated with macrophages/microglia activation and phagocytic activity 42,43 .”
The A53T mutation in α-synuclein enhances pro-inflammatory activation in human microgliaPreprint
Krzisch, M., Yuan, B., Chen, W., Osaki, T., Fu, D., Garrett-Engele, C. M., Svoboda, D. S., Andrykovich, K. R., Sur, M., & Jaenisch, R. (2023) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2023.08.29.555300 · Cited by 2
Role of microglia in stress-induced alcohol intake in female and male micePreprint
Soares, A. R., Garcia‐Rivas, V., Fai, C., Thomas, M. A., Zheng, X., Picciotto, M. R., & Mineur, Y. S. (2024) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2024.06.05.597614 · Cited by 2
Astillero‐Lopez, V., Villar‐Conde, S., González-Rodríguez, M., Flores‐Cuadrado, A., Úbeda‐Bañón, I., Saiz‐Sánchez, D., & Martínez-Marcos, A. (2023) · IBRO Neuroscience Reports · doi:10.1016/j.ibneur.2023.08.680 · Cited by 1
Papain Affects the Percentage and Morphology of Microglia in Hippocampal Neuron–Glial Cultures
Tumozov, I. A., Mal’tseva, V. N., Maiorov, S. A., Kosenkov, A. M., & Gaidin, S. G. (2025) · Brain Sciences · doi:10.3390/brainsci15050442 · Cited by 1
“However, according to a number of studies, its expression may vary depending on experimental conditions, and some researchers consider it a marker of active microglia [33,34].”
Hemati, H., Blanton, M. B., True, H., Koura, J., Khadka, R., Grant, K. A., & Messaoudi, I. (2025) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2025.07.022 · Cited by 2
Propolis Improved Methomyl‐Induced Neurotoxicity in the Developing Brain of Albino Rats
Atallah, M. N., Badawy, G. M., Abdallah, F. S., El‐Gaber, A. S. A., & El‐Borm, H. T. (2025) · Journal of Experimental Zoology Part A Ecological and Integrative Physiology · doi:10.1002/jez.70021 · Cited by 1
The Role of Microglia in the Pathophysiology of Post-Traumatic Stress Disorder
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“Resting microglia exhibit a ramified morphology, whereas reactive microglia typically display an amoeboid morphology [27].”
Focal postnatal deletion of Tsc2 causes epilepsy
McCoy, C., Dusing, M. R., Jerow, L. G., Winstel, G. C., Zhan, F., Rogers, J. L., Wesley, M., Otten, J. B., Danzer, S. C., & LaSarge, C. L. (2025) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2025.1686023 · Cited by 1
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“In the ischemic retina (ROP, DR), inflammation is largely driven by glial activation, where cytokine-producing Iba-1 + microglia accumulate and promote pathologic neovascularization and neuronal loss [88–90].”
Iba, M., Lee, Y., Kwon, S., Horan-Portelance, L., Chang, K., Kim, M., Landeck, N., Rissman, R. A., Lee, S. J., You, S., et al. (2025) · Experimental & Molecular Medicine · doi:10.1038/s12276-025-01564-4 · Cited by 3
Casanova-Pagola, J., Varriano, F., López-Gil, X., Campoy‐Campos, G., Abellí‐Deulofeu, E., García-González, C., López-Bravo, E., Tudela, R., Muñoz‐Moreno, E., Aguado, F., et al. (2025) · iScience · doi:10.1016/j.isci.2025.114381 · Cited by 1
Metadata
- Authors
- Lier, J., Streit, W. J., & Bechmann, I.
- Affiliations
- Leipzig University (DE)
- University of Florida Health (US)
- Corresponding author
- Lier, Julia
- Venue
- Cells
- Publisher
- MDPI AG
- Published
- 2021-08-28
- Volume
- 10
- Issue
- 9
- Pages
- 2236
- ISSN
- 2073-4409 (ISSN-L)
- PMC
- PMC8464670
- OpenAlex
- W3196760175
- Cited by
- 274
- References
- 112
- Citations by year
- 2026: 50 · 2025: 74 · 2024: 90 · 2023: 40 · 2022: 20
- FWCI
- 12.67
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cells (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (submittedVersion, other-oa)
- PubMed Central (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Qucosa (Saxon State and University Library Dresden) (submittedVersion, cc-by)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- microglia, microglial activation, microglial morphology, ramified microglia, amoeboid microglia, microglial senescence, microglial heterogeneity, microglial markers, Iba1, liver disease, Alzheimer's disease, neurodegeneration, brain aging
- MeSH terms
- CD68 Molecule, Animals, Antigens, Differentiation, B-Lymphocyte, Histocompatibility Antigens Class II, Brain, Calcium-Binding Proteins, Humans, Membrane Proteins, Microfilament Proteins, Nerve Tissue Proteins, Phagocytes, Phenotype, Antigens, Differentiation, Myelomonocytic, Signal Transduction, Antigens, CD, Microglia, Neurodegenerative Diseases, Receptors, Purinergic P2Y12
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