The DOI matches its Crossref record; 234 of the 235 references it cites were found in a registry or an index, and 1 are not checked yet.
Microglia-orchestrated neuroinflammation and synaptic remodeling: roles of pro-inflammatory cytokines and receptors in neurodegeneration
Open accessAbstract
Microglia, the innate immune cells of the central nervous system (CNS), play essential roles in maintaining neural homeostasis through dynamic interactions with neurons and other brain structures. While their protective functions are well-established, recent studies have illuminated the detrimental consequences of sustained microglial activation in the context of neurodegeneration. In particular, overactivated microglia contribute to neuroinflammation and induce synaptic alterations through the release of pro-inflammatory cytokines and engagement of specific receptors. These interactions disrupt synaptic structure and function, compromising connectivity, plasticity, and cognitive processes. Notably, neuronal synapses are primary targets of such inflammation-driven dysfunction, where prolonged exposure to cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor- α (TNF-α), and signaling via receptor systems including cluster of differentiation-200 (CD200)/CD200 receptor (CD200R), C-X3-C motif chemokine ligand 1 (CX3CL1)/CX3C receptor 1 (CX3CR1), colony-stimulating factor 1 (CSF1)/CSF1 receptor (CSF1R), and interferon- γ (IFN-γ)/IFN-γ receptor (IFN-γR), lead to impaired learning, excitotoxicity, and neurodegenerative progression. This review synthesizes emerging evidence on the mechanisms by which microglia-mediated immune responses regulate synaptic remodeling, emphasizing the roles of pro-inflammatory cytokines and their receptors in neurodegenerative disorders.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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 source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This provides a plausible link between EDC-induced neuroinflammation and large-scale disturbances in connectivity and plasticity (Lara de Deus et al., 2025; Yang et al., 2025).”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Yang et al., 2025
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Microglia are essential for synaptic pruning and circuit refinement during development, but chronic inflammatory activation can shift them toward maladaptive synapse elimination and aberrant remodeling.”
From Environmental endocrine disruptors at the synapse: mechanisms linking chemical exposure to cognitive and behavioral dysfunction (2026) · cites this paper as Yang et al., 2025
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
Items 201–235 of 235
O'Neill, E., Kwok, B., Day, J. S., Connor, T. J., & Harkin, A. (2016) · Pharmacology Research & Perspectives · doi:10.1002/prp2.195 · Cited by 20
van der Maten, G., Henck, V., Wieloch, T. W., & Ruscher, K. (2017) · BMC Neuroscience · doi:10.1186/s12868-016-0325-0 · Cited by 20
Wang, X., Ma, C., Liu, C., Li, G., Zhao, D., & Han, D. (2019) · Frontiers in Neurology · doi:10.3389/fneur.2019.00684 · Cited by 20
Self-citationTian, Y., Xiao, X., Liu, W., Cheng, S., Qian, N., Wang, L., Liu, Y., Ai, R., & Zhu, X. (2024) · Molecular Brain · doi:10.1186/s13041-024-01081-x · Cited by 20
Tumor necrosis factor alpha mediates neuromuscular synapse elimination
Fu, X.-Q., Peng, J., Wang, A., & Luo, Z. (2020) · Cell Discovery · doi:10.1038/s41421-020-0143-5 · Cited by 19
Lewen, A., Ta, T., Cesetti, T., Hollnagel, J., Papageorgiou, I. E., Chausse, B., & Kann, O. (2020) · Journal of Neuroscience Research · doi:10.1002/jnr.24689 · Cited by 18
Bertot, C., Groc, L., & Avignone, E. (2019) · Neuroscience · doi:10.1016/j.neuroscience.2019.03.006 · Cited by 17
Klein, H., Schäfer, M. K.-H., Bennett, D. A., Schwender, H. R., & Jager, P. L. D. (2020) · PLoS Computational Biology · doi:10.1371/journal.pcbi.1007771 · Cited by 17
Zhou, R., & Bickler, P. E. (2016) · Anesthesia & Analgesia · doi:10.1213/ane.0000000000001698 · Cited by 16
Milinkeviciute, G., Chokr, S. M., Castro, E. M., & Cramer, K. S. (2021) · The Journal of Comparative Neurology · doi:10.1002/cne.25150 · Cited by 16
Omoyinmi, E., Hamaoui, R., Bryant, A., Jiang, M. C., Athigapanich, T., Eleftheriou, D., Hubank, M. J. F., Brogan, P. A., & Woo, P. M. (2016) · Pediatric Rheumatology · doi:10.1186/s12969-016-0067-7 · Cited by 16
Sung, C., Wen, Z., Feng, C., Chen, C., Huang, S., Chen, N., Chen, W.-F., & Wong, C. (2017) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.12705 · Cited by 15
Physiological Implications of Microglia–Synapse Interactions
Wake, H., Horiuchi, H., Kato, D., Moorhouse, A. J., & Nabekura, J. (2019) · Methods in molecular biology · doi:10.1007/978-1-4939-9658-2_6 · Cited by 15
Pan, E., Zhao, Z., & McNamara, J. O. (2018) · Journal of Neurophysiology · doi:10.1152/jn.00669.2018 · Cited by 14
Impact of Chronic BDNF Depletion on GABAergic Synaptic Transmission in the Lateral Amygdala
Meis, S., Endres, T., Munsch, T., & Leßmann, V. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20174310 · Cited by 14
Huang, L., Lafaille, J. J., & Yang, G. (2021) · Developmental Neurobiology · doi:10.1002/dneu.22827 · Cited by 13
Self-citationInterleukin 6 Dependent Synaptic Plasticity in a Social Defeat-Susceptible Prefrontal Cortex Circuit
Esquivel‐Rendon, E., Vargas‐Mireles, J., Cuevas‐Olguin, R., Miranda‐Morales, M., Acosta-Mares, P., García‐Oscos, F., Pineda, J. C., Salgado, H., Rose‐John, S., & Atzori, M. (2019) · Neuroscience · doi:10.1016/j.neuroscience.2019.07.002 · Cited by 12
Yang, G., Tong, Y., Wang, X., Zhao, C., Ba, Z., Ahelijiang, R., Liu, X., Gao, W., Zhao, Y., Gu, Y., et al. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1185570 · Cited by 12
Self-citationThe double‐edged sword of IFN‐γ‐dependent immune‐based therapies
John, L. B., & Darcy, P. K. (2016) · Immunology and Cell Biology · doi:10.1038/icb.2016.37 · Cited by 11
Cuevas‐Olguin, R., Esquivel‐Rendon, E., Vargas‐Mireles, J., García‐Oscos, F., Miranda‐Morales, M., Salgado, H., Rose‐John, S., & Atzori, M. (2017) · Synapse · doi:10.1002/syn.21984 · Cited by 11
IL-6 deficiency attenuates p53 protein accumulation in aged male mouse hippocampus
Bialuk, I., Cieślińska, M., Kowalczuk, O., Bonda, T. A., Nikliński, J., & Winnicka, M. M. (2019) · Biogerontology · doi:10.1007/s10522-019-09841-2 · Cited by 11
Interleukin-1β Alters Hebbian Synaptic Plasticity in Multiple Sclerosis
Bassi, M. S., Buttari, F., Nicoletti, C. G., Mori, F., Gilio, L., Simonelli, I., Paolis, N. D., Marfia, G. A., Furlan, R., Finardi, A., et al. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21196982 · Cited by 11
Garad, M., Edelmann, E., & Leßmann, V. (2021) · Scientific Reports · doi:10.1038/s41598-021-87769-9 · Cited by 11
Yang, X., Li, T., Liu, J., Sun, H. B., Cheng, L., Song, X., Han, Z., Luo, H., Han, W., Xie, L., et al. (2023) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.14352 · Cited by 10
You, Y., An, D., Wan, Y., Zheng, B.-X., Dai, H., Zhang, S., Zhang, X., Wang, R., Shi, P. D., Jin, M., et al. (2024) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-023-05111-0 · Cited by 9
Kodali, M., Madhu, L. N., Somayaji, Y., Attaluri, S., Huard, C., Panda, P. K., Shankar, G., Rao, S.-M., Shuai, B., Gonzalez, J. J., et al. (2024) · bioRxiv · doi:10.1101/2024.07.11.603157 · Cited by 9
Rapamycin-Sensitive Late-LTP is Enhanced in the Hippocampus of IL-6 Transgenic Mice
Engberink, A. H. O. O., Hernandez, R. V., Graan, P. N. E. D., & Gruol, D. L. (2017) · Neuroscience · doi:10.1016/j.neuroscience.2017.10.040 · Cited by 8
Kleidonas, D., & Vlachos, A. (2021) · Cells · doi:10.3390/cells10113232 · Cited by 8
Yu, Q., Liu, M., Dai, W., Xiong, Y., Mu, X., Xia, M., Li, Y., Ma, S., Su, Y., Wu, J., et al. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.974905 · Cited by 8
Neuroimmune interactions with binge alcohol drinking in the cerebellum of IL-6 transgenic mice
Gruol, D. L., Calderon, D., French, K., Melkonian, C., Huitrón‐Reséndiz, S., Cates‐Gatto, C., & Roberts, A. J. (2023) · Neuropharmacology · doi:10.1016/j.neuropharm.2023.109455 · Cited by 8
The role of P2X4R in regulating CA1 hippocampal synaptic impairment in LPS-induced depression
Wei, L., Yu, X., Chen, H., & Du, Y. (2024) · Journal of Affective Disorders · doi:10.1016/j.jad.2024.07.052 · Cited by 8
Gellner, A., Reis, J., Fiebich, B. L., & Fritsch, B. (2023) · European Journal of Neuroscience · doi:10.1111/ejn.16206 · Cited by 7
Priming of hippocampal microglia by IFN-γ/STAT1 pathway impairs social memory in mice
He, H., Zhang, X., He, H., Xiao, C., Xu, G., Li, L., Li, L., Yang, C., Zhou, T., You, Z., et al. (2024) · International Immunopharmacology · doi:10.1016/j.intimp.2024.112191 · Cited by 7
Tong, L., Chen, G., Liu, T., Wang, L., Zhang, H., Chen, F., Zhang, S., & Du, D. (2023) · Journal of Hypertension · doi:10.1097/hjh.0000000000003470 · Cited by 6
Stefano, G. B., Büttiker, P., Michaelsen, M. M., & Esch, T. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26125491 · Cited by 6
Flagged first, then by citations
Research works printed but not linked: 2
- Han, 2016, Seizure induced synaptic plasticity alteration in hippocampus is mediated by IL-1β receptor through PI3K/Akt pathway, Am. J. Transl. Res., 15, 4499
- Ngwa, 2019, CD200-CD200R signaling and diseases: a potential therapeutic target, Int J Physiol Pathophysiol Pharmacol, 11, 297
Cited by
Sorted by citations
Rethinking early Alzheimer’s disease: An impaired internal model updating disorder?
Antonioni, A. (2026) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2026.106790 · Cited by 8
Yoo, Y., Baek, S. Y., Lee, H., Lee, J., Lee, H., Lee, H., Ma, H., Kim, Y., Choi, H., Lee, J. T., et al. (2026) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.5c02981 · Cited by 6
Ferreira, A. F. F., Santos-Silva, A. C., Muratori, B. G., & Britto, L. R. G. (2026) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2026.1733682 · Cited by 5
Yen, C., & Chiang, M. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27021080 · Cited by 4
Messina, A., Bella, F., Maccarone, G., Avincola, G., & Signorelli, M. S. (2026) · Journal of Psychiatric Research · doi:10.1016/j.jpsychires.2026.01.007 · Cited by 3
Metadata
- Authors
- Yang, G., Xu, X., Gao, W., Wang, X., Zhao, Y., & Xu, Y.
- Affiliations
- Shanghai University of Traditional Chinese Medicine (CN)
- Corresponding author
- Zhao, Yan
- Xu, Ying
- Venue
- Frontiers in Cellular Neuroscience
- Publisher
- Frontiers Media SA
- Published
- 2025-11-10
- Volume
- 19
- Pages
- 1700692-1700692
- ISSN
- 1662-5102 (ISSN-L)
- PMC
- PMC12641016
- OpenAlex
- W4416096320
- Cited by
- 85
- References
- 234
- Citations by year
- 2026: 83 · 2025: 2
- FWCI
- 8.24
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Cellular Neuroscience (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Natural Science Foundation of China
- China Postdoctoral Science Foundation
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, neuroinflammation, synaptic remodeling, inflammatory cytokines, neurodegeneration, IL-1β, interleukin-6, TNF-α, CX3CL1/CX3CR1, excitotoxicity, learning disabilities, neurodegenerative diseases
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 ›
Are you an author, or do you see a problem with this page? Request a review
