The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index.
Sustained hippocampal IL-1β overexpression mediates chronic neuroinflammation and ameliorates Alzheimer plaque pathology
Open accessAbstract
Neuroinflammation is a conspicuous feature of Alzheimer disease (AD) pathology and is thought to contribute to the ultimate neurodegeneration that ensues. IL-1 beta has emerged as a prime candidate underlying this response. Here we describe a transgenic mouse model of sustained IL-1 beta overexpression that was capable of driving robust neuroinflammation lasting months after transgene activation. This response was characterized by astrocytic and microglial activation in addition to induction of proinflammatory cytokines. Surprisingly, when triggered in the hippocampus of the APPswe/PS1dE9 mouse model of AD, 4 weeks of IL-1 beta overexpression led to a reduction in amyloid pathology. Congophilic plaque area fraction and frequency as well as insoluble amyloid beta 40 (A beta 40) and A beta 42 decreased significantly. These results demonstrate a possible adaptive role for IL-1 beta-driven neuroinflammation in AD and may help explain recent failures of antiinflammatory therapeutics for this disease.
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
“previous studies demonstrated that IL1 overexpression enhances A clearance.9,53”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [9]
Experimental — accuracy not yet measuredThe 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 is consistent with our previously published data showing that IL-1β does not influence Aβ production [4, 6, 7, 28].”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [4]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“For amyloid pathology, there is data that activated micro/astroglia enhances Aβ phagocytosis [60, 62, 71]”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [62]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Recent studies demonstrated that overexpression of IL1, an inflammatory cytokine leads to reduced A pathology in mouse models of AD. 9,53”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“Various genetically modified mouse models have convincingly demonstrated the role for other chemokines/cytokine pathways in altering the accumulation of mononuclear phagocytes (monocytes, macrophages, and microglia) and A pathology, including CCR2 59 and IL1.9”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“numerous other studies have suggested that altering the proliferation, 58 signaling, 8,9,11 and migration 7,59 of microglia directly impact development of A pathology.”
From CX3CR1 Deficiency Alters Microglial Activation and Reduces Beta-Amyloid Deposition in Two Alzheimer's Disease Mouse Models (2010) · cites this paper as [9]
The cited source says what the claim attributes to it.
In the citing paper
“As previously described [28], APP/PS1 mice transduced with rAAV2-IL-1β showed significant reductions in hippocampal amyloid plaques compared to mice treated with rAAV2-Phe, as determined by immunohistochemical (IHC) analysis using both 6E10 staining and MX04 (Fig. 1b)”
From IL-1β-driven amyloid plaque clearance is associated with an expansion of transcriptionally reprogrammed microglia (2019) · cites this paper as [4]
The cited source says what the claim attributes to it.
In the citing paper
“Hippocampal expression of IL-1β was shown to robustly reduce plaques in the APP/PS1 model and 3xTg-AD model but worsened tauopathy in the 3xTg-AD model [62, 63].”
From Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways (2022) · cites this paper as [62]
In the citing paper
“In turn, increased cytokines, such as interleukin-1, can influence Aβ uptake (Mrak and Griffin, 2000; Shaftel et al., 2007).”
From LC3-Associated Endocytosis Facilitates β-Amyloid Clearance and Mitigates Neurodegeneration in Murine Alzheimer’s Disease (2019) · cites this paper as Shaftel et al., 2007
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
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Cre reporter strains produced by targeted insertion of EYFP and ECFP into the ROSA26 locus
Srinivas, S., Watanabe, T., Lin, C.-S., William, C. M., Tanabe, Y., Jessell, T. M., & Costantini, F. (2001) · BMC Developmental Biology · doi:10.1186/1471-213x-1-4 · Cited by 3,121
Systematic meta-analyses of Alzheimer disease genetic association studies: the AlzGene database
Bertram, L., McQueen, M. B., Mullin, K., Blacker, D., & Tanzi, R. E. (2007) · Nature Genetics · doi:10.1038/ng1934 · Cited by 1,857
Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease.
Griffin, W. S., Stanley, L. C., Ling, C., White, L., MacLeod, V, Perrot, L. J., White, C. L., & Araoz, C. (1989) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.86.19.7611 · Cited by 1,777
Jankowsky, J. L., Fadale, D. J., Anderson, J., Xu, G. M., Gonzales, V., Jenkins, N. A., Copeland, N. G., Lee, M. K., Younkin, L. H., Wagner, S. L., et al. (2004) · Human Molecular Genetics · doi:10.1093/hmg/ddh019 · Cited by 1,575
Simard, A. R., Soulet, D., Gowing, G., Julien, J.-P., & Rivest, S. (2006) · Neuron · doi:10.1016/j.neuron.2006.01.022 · Cited by 1,265
Interleukin-1 and neuronal injury
Allan, S. M., Tyrrell, P. J., & Rothwell, N. J. (2005) · Nature Reviews Immunology · doi:10.1038/nri1664 · Cited by 992
Ibuprofen Suppresses Plaque Pathology and Inflammation in a Mouse Model for Alzheimer's Disease
Lim, G. P., Yang, F., Chu, T., Chen, P., Beech, W. K., Teter, B., Tran, T., Ubeda, O. J., Ashe, K. H., Frautschy, S. A., et al. (2000) · Journal of Neuroscience · doi:10.1523/jneurosci.20-15-05709.2000 · Cited by 876
McGeer, P. L., Itagaki, S., Tago, H., & McGeer, E. G. (1987) · Neuroscience Letters · doi:10.1016/0304-3940(87)90696-3 · Cited by 836
Co-expression of multiple transgenes in mouse CNS: a comparison of strategies
Jankowsky, J. L., Slunt, H. H., Ratovitski, T., Jenkins, N. A., Copeland, N. G., & Borchelt, D. R. (2001) · Biomolecular Engineering · doi:10.1016/s1389-0344(01)00067-3 · Cited by 746
Flagged first, then by citations
Cited by
Sorted by citations
Items 301–400 of 427
Methyl Jasmonate: Behavioral and Molecular Implications in Neurological Disorders
Aluko, O. M., Iroegbu, J. D., Ijomone, O. M., & Umukoro, S. (2021) · Clinical Psychopharmacology and Neuroscience · doi:10.9758/cpn.2021.19.2.220 · Cited by 14
Srinivasan, S., Kancheva, D., Ren, S. D., Saito, T., Jans, M., Boone, F., Vandendriessche, C., Paesmans, I., Maurin, H., Vandenbroucke, R. E., et al. (2024) · Frontiers in Immunology · doi:10.3389/fimmu.2024.1323409 · Cited by 16
Calvillo, M., Díaz, A., Limón, I. D., Mayoral, M. Á., Chánez‐Cárdenas, M. E., Zenteno, E., Montaño, L. F., Guevara, J., & Espinosa, B. (2013) · Neuropeptides · doi:10.1016/j.npep.2013.06.002 · Cited by 14
The orphan nuclear receptor TLX regulates hippocampal transcriptome changes induced by IL-1β
Ó’Léime, C. S., Hoban, A. E., Hueston, C. M., Stilling, R. M., Moloney, G. M., Cryan, J. F., & Nolan, Y. M. (2018) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2018.03.006 · Cited by 13
IL-1R-/- alleviates cognitive deficits through microglial M2 polarization in AD mice
Wang, H., Peng, G., Wang, B., Yin, H., Fang, X., He, F., Zhao, D., Liu, Q., & Shi, L. (2020) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2019.11.020 · Cited by 13
Whole-food diet worsened cognitive dysfunction in an Alzheimer's disease mouse model
Parrott, M. D., Winocur, G., Bazinet, R. P., David, W. L., & Greenwood, C. E. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.08.013 · Cited by 13
Interleukin 6 and 10 Serum Levels and Genetic Polymorphisms in Children with Down Syndrome
Mattos, M. F., Biselli-Chicote, P. M., Biselli, J. M., Assembleia, T. L. D. S., Goloni‐Bertollo, E. M., & Pavarino, É. C. (2018) · Mediators of Inflammation · doi:10.1155/2018/6539548 · Cited by 13
Gómez‐Nicola, D., & Perry, V. H. (2014) · Springer eBooks · doi:10.1007/978-1-4939-1429-6_18 · Cited by 13
cFLIP is critical for oligodendrocyte protection from inflammation
Tanner, D. C., Campbell, A., O’Banion, M. K., Noble, M., & Mayer-Pröschel, M. (2015) · Cell Death and Differentiation · doi:10.1038/cdd.2014.237 · Cited by 13
Self-citationInterlacing the relevance of caspase activation in the onset and progression of Alzheimer’s disease
Dhage, P. A., Sharbidre, A. A., & Magdum, S. M. (2022) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2022.11.008 · Cited by 12
Baranger, K., van Gijsel‐Bonnello, M., Stephan, D., Carpentier, W., Rivera, S., Khrestchatisky, M., Gharib, B., Reggi, M. L. D., & Benech, P. (2019) · Neurotherapeutics · doi:10.1007/s13311-019-00754-z · Cited by 13
Characterization of inflammatory biomarkers and candidates for diagnosis of Alzheimer’s disease
Bagyinszky, E., Youn, Y. C., An, S. S. A., & Kim, S. (2014) · BioChip Journal · doi:10.1007/s13206-014-8301-1 · Cited by 12
Effects of Microglial Cytokines on Alzheimer’s Disease-Related Phenomena
Ji, Y., Wang, X., Kalicki, C. H., Menta, B. W., Baumgardner, M., Koppel, S. J., Weidling, I. W., Ortiz, J. P., Wilkins, H., & Swerdlow, R. H. (2019) · Journal of Alzheimer s Disease · doi:10.3233/jad-180820 · Cited by 12
Lykhmus, O., Kalashnyk, O., Koval, L., Voytenko, L. P., Uspenska, K., Комісаренко, С. В., Deryabina, О. G., Shuvalova, N. S., Кордюм, В. А., Ustymenko, A., et al. (2019) · Neuroscience · doi:10.1016/j.neuroscience.2019.06.004 · Cited by 12
Neuroinflammation to neurodegeneration: Boulevard of broken nerves
Attiq, A., Afzal, S., Raman, H., & Ahmad, W. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.115015 · Cited by 12
Kumar, P., Mathew, S., Gamage, R. V., Bodkin, F., Doyle, K., Rosetti, I., Wagnon, I. M., Zhou, X., Raju, R., Gyengési, E., et al. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241311086 · Cited by 12
Giunti, E., Collu, R., Daley, S. A., Querfurth, H. W., Morin, P., Killick, R., Melamed, R., & Xia, W. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230551 · Cited by 12
Temporal-logic analysis of microglial phenotypic conversion with exposure to amyloid-β
Anastasio, T. J. (2014) · Molecular BioSystems · doi:10.1039/c4mb00457d · Cited by 11
Ma, X., Prokopenko, D., Wang, N., Aikawa, T., Choi, Y., Zhang, C. M., Lei, D., Ren, Y., Kawatani, K., Starling, S. C., et al. (2025) · Neurobiology of Disease · doi:10.1016/j.nbd.2025.106813 · Cited by 10
Suk, K. (2026) · Experimental Neurology · doi:10.1016/j.expneurol.2026.115737 · Cited by 11
Ryan, K. M., Griffin, É. W., Ryan, K. J., Tanveer, R., Vanattou‐Saïfoudine, N., McNamee, E. N., Fallon, E., Heffernan, S., Harkin, A., & Connor, T. J. (2016) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2016.02.023 · Cited by 11
Marinelli, L., Fornasari, E., Stefano, A. D., Türkez, H., Genovese, S., Epifano, F., Biase, G. D., Costantini, E., D’Angelo, C., Reale, M., et al. (2018) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2018.11.057 · Cited by 10
Arosio, B., Rossi, P. D., Ferri, E., Consorti, E., Ciccone, S., Lucchi, T. A., & Montano, N. (2025) · Experimental Gerontology · doi:10.1016/j.exger.2025.112692 · Cited by 9
Diaz, M. F., Horton, P. D., Kumar, A., Livingston, M. K., Mohammadalipour, A., Xue, H., Skibber, M. A., Ewere, A., Furman, N. E. T., Aroom, K., et al. (2020) · Scientific Reports · doi:10.1038/s41598-020-67723-x · Cited by 9
Biological determinants of blood‐based cytokines in the Alzheimer's disease clinical continuum
Galgani, A., Vergallo, A., Campese, N., Lombardo, F. P., Pavese, N., Petrozzi, L., LoGerfo, A., Franzini, M., Cecchetti, D., Puglisi‐Allegra, S., et al. (2022) · Journal of Neurochemistry · doi:10.1111/jnc.15686 · Cited by 10
Malm, T., Magga, J. M., & Koıstınaho, J. (2012) · Current Translational Geriatrics and Experimental Gerontology Reports · doi:10.1007/s13670-011-0004-z · Cited by 9
Ni, J., & Wu, Z. (2021) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2021.638686 · Cited by 9
Neuroinflammation: an unfortunate term to describe schizophrenia
Llorca-Bofí, V., Parellada, E., Morén, C., Sellgren, C. M., & Bioque, M. (2026) · Molecular Psychiatry · doi:10.1038/s41380-026-03450-5 · Cited by 8
Mendoza‐Marí, Y., Rai, V., Radwan, M. M., Brazdzionis, J., Connett, D. A., Miulli, D. E., & Agrawal, D. K. (2024) · Journal of Surgery and Research · doi:10.26502/jsr.10020338 · Cited by 9
Liu, B., Luo, W., Huang, L., Wei, C., Huang, X., Liu, J., Tao, R., Mo, Y., & Li, X. (2024) · American Journal of Alzheimer s Disease & Other Dementias® · doi:10.1177/15333175241238577 · Cited by 11
Verbeeck, C., Carrano, A., Chakrabarty, P., Jankowsky, J. L., & Das, P. (2017) · American Journal Of Pathology · doi:10.1016/j.ajpath.2017.08.010 · Cited by 8
Deletion of MyD88 in astrocytes prevents β‐amyloid‐induced neuropathology in mice
Huat, T. J., Onraet, T., Camats‐Perna, J., Newcombe, E. A., Ngo, K. C., Sue, A. N., Mirzaei, M., LaFerla, F. M., & Medeiros, R. (2022) · Glia · doi:10.1002/glia.24285 · Cited by 8
Glutamate Excitotoxicity in the Cerebellum Mediated by IL-1β
Mohebiany, A. N., & Schneider, R. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.3946-13.2013 · Cited by 8
Modulation of adult hippocampal neurogenesis by interleukin 1 signaling
Smirnova, M. I., & Quan, N. (2025) · Neurobiology of Sleep and Circadian Rhythms · doi:10.1016/j.nbscr.2025.100123 · Cited by 8
Askarova, S., Sitdikova, K., Kassenova, A., Chaprov, K., Svirin, E. P., Tsoy, A., de Munter, J., Вячеславовна, Г. А., Litavrin, A., Deykin, A. V., et al. (2025) · Antioxidants · doi:10.3390/antiox14070834 · Cited by 7
Dembitskaya, Y., & Popov, A. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-025-01706-7 · Cited by 8
Calcines-Rodríguez, L., Noyes-Martel, N., Becker, J. D., Nguyen, S. K., Osabutey, M., Trojanczyk, L., Majewska, A. K., & O’Banion, M. K. (2025) · Journal of Neuroinflammation · doi:10.1186/s12974-025-03659-1 · Cited by 8
Self-citationGardner, R. S., Kyle, M. M., Hughes, K., & Zhao, L. (2024) · Biomolecules · doi:10.3390/biom14070827 · Cited by 7
Bi, F., Bai, Y. M., Zhang, Y., Shi, M., & Liu, W. (2022) · Experimental and Therapeutic Medicine · doi:10.3892/etm.2022.11707 · Cited by 7
Chronic Diseases and Influenza Vaccines
Lian, R., Zhang, H., An, Y., & Chen, Z. (2025) · Vaccines · doi:10.3390/vaccines13090936 · Cited by 6
Dental X-ray exposure and Alzheimer’s disease: A hypothetical etiological association
Rodgers, C. C. (2011) · Medical Hypotheses · doi:10.1016/j.mehy.2011.03.016 · Cited by 6
The role of IL-1 family of cytokines in the pathogenesis and therapy of Alzheimer’s disease
Li, C., Zhang, X., Wang, Y., Cheng, L., Li, C., & Yu, X. (2024) · Inflammopharmacology · doi:10.1007/s10787-024-01534-8 · Cited by 6
Sokolik, V. V., & Maltsev, A. V. (2015) · Biomeditsinskaya Khimiya · doi:10.18097/pbmc20156103373 · Cited by 6
Li, J., Li, C., Subedi, U., Subedi, P., Panchatcharam, M., & Sun, H. (2024) · Cells · doi:10.3390/cells13232007 · Cited by 5
“Methyl jasmonate: bridging plant defense mechanisms and human therapeutics”
Sharma, G., Badruddeen, B., Akhtar, J., Khan, M. I., Ahmad, M. K., & Sharma, P. K. (2025) · Naunyn-Schmiedeberg s Archives of Pharmacology · doi:10.1007/s00210-024-03752-x · Cited by 5
Clements, A. E. B., Leiferman, E. M., Chamberlain, C. S., Vanderby, R., & Murphy, W. L. (2018) · Advanced Therapeutics · doi:10.1002/adtp.201800048 · Cited by 5
Ablinger, I., Dressel, K., Rott, T., Lauer, A. A., Tiemann, M., Batista, J. P., Taddey, T., Grimm, H. S., & Grimm, M. O. W. (2022) · Biomedicines · doi:10.3390/biomedicines10112922 · Cited by 5
The Role of T Cells in Alzheimer's Disease Pathogenesis
Zhao, J., Wang, X., He, Y., Xu, P., Lai, L., Chung, Y., & Pan, X. (2023) · Critical Reviews in Immunology · doi:10.1615/critrevimmunol.2023050145 · Cited by 4
Rice, M., Nuovo, G. J., Sawant, D. B., Mishra, A., & Tili, E. (2023) · Molecular Neurobiology · doi:10.1007/s12035-023-03822-w · Cited by 4
Ma, S., Xu, C.-C., Dong, Y.-C., Li, C., & Shang, Y. (2024) · Combinatorial Chemistry & High Throughput Screening · doi:10.2174/0113862073265060231127054325 · Cited by 4
Zhu, A., Xi, A., Li, G., Li, Y., Liao, B., Zhong, X., Zhou, J., Gu, S., Yu, M., & Yide, C. (2012) · Journal of Behavioral and Brain Science · doi:10.4236/jbbs.2012.21009 · Cited by 4
Kokhan, V. S., Андреевич, А. Р., Anokhin, P. K., & Shamakina, I. Y. (2025) · Biochemistry (Moscow) · doi:10.1134/s0006297924604453 · Cited by 3
Arslan, S. O., Uysal, F., Koç, A., & Çam, S. A. (2025) · Çukurova medical journal (Online)/Çukurova medical journal · doi:10.17826/cumj.1588353 · Cited by 3
Dual role of innate immune activation in cerebral small vessel disease
Peng, Y., Sun, Y., Song, X., Jin, C. J., Yin, X., & Zheng, X. (2025) · International Immunopharmacology · doi:10.1016/j.intimp.2025.115178 · Cited by 3
Wu, M., Chen, Y., Yao, W., Zhou, S., Xie, Z., Tao, Y., Zhong, Y., & Ma, W. (2025) · Scientific Reports · doi:10.1038/s41598-025-91785-4 · Cited by 3
Liu, T., & Li, X. (2025) · Journal of Biochemical and Molecular Toxicology · doi:10.1002/jbt.70460 · Cited by 3
Sokolik, V. V., & Maltsev, A. V. (2015) · Biochemistry (Moscow) Supplement Series B Biomedical Chemistry · doi:10.1134/s1990750815040058 · Cited by 3
Glial Activation and Synaptic Neurotoxicity in Alzheimer's disease: A Focus on Neuroinflammation
Rai, S., Kamat, P. K., Nath, C., & Shukla, R. (2014) · Pharmacologia · doi:10.5567/pharmacologia.2014.286.297 · Cited by 3
The involvement of neuronal chloride transporter deficiencies in epilepsy
Sullivan, B. J., & Kadam, S. D. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-815318-5.00014-5 · Cited by 3
Immunotherapy: An Approach to Treat Alzheimer’s Disease and Autism Spectrum Disorder
Maarfi, F., Hasan, Z., Khanam, A., Husain, A., Khan, M. H., & Khan, M. Y. (2021) · Springer eBooks · doi:10.1007/978-981-16-4558-7_11 · Cited by 3
Rodriguez, L. C., Noyes-Martel, N., Becker, J. D., Majewska, A. K., & O’Banion, M. K. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.03.28.646050 · Cited by 3
Self-citationCorley, C. L., Swinton, C., McElory, T., Sridharan, B., Thomas, J. J., Cronin, B., Sridharan, V., Robeson, M. S., & Allen, A. R. (2025) · Frontiers in Microbiomes · doi:10.3389/frmbi.2025.1486757 · Cited by 2
Regulated intramembrane proteolysis, innate immunity and therapeutic targets in Alzheimer’s disease
Hurst, T. P., Coleman-Vaughan, C., Patwal, I., & McCarthy, J. V. (2016) · AIMS molecular science · doi:10.3934/molsci.2016.2.138 · Cited by 2
The contribution of inflammation to Alzheimer's disease in Down syndrome
Martini, A. C., Kloske, C. M., Wilcock, D. M., & Head, E. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-818845-3.00016-5 · Cited by 2
Models of neuroinflammation for the assessment of kappa-opioid receptor ligands
Kalitin, K. Y., Спасов, А. А., & Mukha, O. Y. (2023) · Pharmacy & Pharmacology · doi:10.19163/2307-9266-2023-11-1-4-18 · Cited by 2
Kim, M. J., Kim, J. H., Lee, S., Cho, E. J., & Kim, H. Y. (2020) · Journal of Applied Biological Chemistry · doi:10.3839/jabc.2020.038 · Cited by 3
Choi, J.-H., Lee, E.-B., Jang, H., Park, Y., & Lee, S. H. (2021) · Korean Journal of Medicinal Crop Science · doi:10.7783/kjmcs.2021.29.5.328 · Cited by 1
Inconsistent Effects of Glatiramer Acetate Treatment in the 5xFAD Mouse Model of Alzheimer’s Disease
Karaahmet, B., Olschowka, J. A., & O’Banion, M. K. (2023) · Pharmaceutics · doi:10.3390/pharmaceutics15071809 · Cited by 1
Self-citationKokhan, V. S., Nesterov, M. S., & Levashova, A. I. (2023) · Doklady Biological Sciences · doi:10.1134/s0012496623700424 · Cited by 1
Hocaoğlu, N., Korkmaz, N. D., Elibol, B., Karakayalı, Z. C., Uşak, Ş. T., & Gürsoy, A. E. (2024) · Turkish Journal of Immunology · doi:10.4274/tji.galenos.2024.40427 · Cited by 1
Koller, E. J., McFarland, K. N., Angelle, C., Howard, J. C., Ryu, D., Dillon, K. D., Erquizi, A., Beheray, M., Cruz, E. G. D. L., Cruz, P. E., et al. (2025) · Acta Neuropathologica Communications · doi:10.1186/s40478-025-01968-3 · Cited by 1
New Perspectives in Nuclear Neurology for the Evaluation of Parkinson's Disease
Benadiba, M., Luurtsema, G., Tumas, V., Buchpiguel, C. A., & Busatto, G. F. (2013) · Journal of Parkinson s Disease · doi:10.3233/jpd-130207 · Cited by 1
Immunopathology of the Nervous System
Remick, A. K., Pershing, M. L., Papenfuss, T. L., Lanigan, L. G., Beck, M. J., & Toot, J. (2017) · Molecular and integrative toxicology · doi:10.1007/978-3-319-47385-7_5 · Cited by 1
Lee, K. M., Kim, S., Tian, Y., Jung, S. M., Chang, Y., Rhee, H. Y., Park, S., Ryu, C., Lee, W.-I., Kim, E. J., et al. (2024) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2024.1388654 · Cited by 1
Novel Somatostatin Receptor Subtype‐4 Agonist Mitigates Microglia Inflammatory Activation
Silwal, A., Mobayen, S., Crider, A. M., Neumann, W. L., House, A., Umbaugh, D. S., Bhandari, S., Sandoval, K. E., & WITT, K. A. (2019) · The FASEB Journal · doi:10.1096/fasebj.2019.33.1_supplement.501.3 · Cited by 1
Neuroinflammation in Alzheimer's Disease Continuum
Sag, A. T., & Yemişçi, M. (2020) · Neurological Sciences and Neurophysiology · doi:10.4103/nsn.nsn_190_20 · Cited by 1
Heparan Sulfate in the Amyloidosis and Inflammation of Alzheimer’s Disease
O′Callaghan, P. W. (2011) · KTH Publication Database DiVA (KTH Royal Institute of Technology) · Cited by 1
Influence of Selected Diets on Neural Insulin Activity and Cognitive Function
Parrott, M. D. (2014) · TSpace (University of Toronto) · Cited by 1
Jackman, N. A. (2013) · OpenCommons at University of Connecticut (University of Connecticut)
Characterization of Envelope-Specific Antibody Response Elicited by HIV-1 Vaccines: A Dissertation
Chen, Y. (2015) · eScholarship@UMassChan · doi:10.13028/m2z88m
Mikroglia bei Alzheimer-Demenz
Wiltfang, J. (2014) · Nervenheilkunde · doi:10.1055/s-0038-1627748
Sarlus, H. (2015) · Figshare
Microglia in the Alzheimers brain: a help or a hindrance?
Vollert, C. T., & Eriksen, J. L. (2014) · AIMS neuroscience · doi:10.3934/neuroscience.2014.3.210
Manipulating Phagocyte Activity in Alzheimer's Disease
Combs, C. K. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-090896
Whalen, M. (2011) · eScholarship@UMassChan · doi:10.13028/eqr8-hw89
Using TUDCA to treat Alzheimer's disease after pathology onset in APP/PS1 mice
Dionísio, P. (2014) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT)
Using TUDCA to treat Alzheimer's disease after pathology onset in APP/PS1 mice
Farmácia, F. D. (2014)
Exploring new possible targets in Methamphetamine exposure
Ribeiro, J. A. M. (2016) · Portuguese National Funding Agency for Science, Research and Technology (RCAAP Project by FCT) · doi:10.34626/pm3c-7e90
Receptor Expression 7 Requires P2X β Activation of Microglia by Amyloid
Trabace, L., Idzko, M., Falzoni, S., Fellin, R., Sanz, J. M., Chiozzi, P., & Ferrari, D. (2012)
O’Leary, J. D. (2017) · Cork Open Research Archive (University College Cork, Ireland)
Investigating the role of normal and abnormal beta-amyloid processing in cognition
Freeman, T. J. (2019) · ORCA Online Research @Cardiff (Cardiff University)
Joppe, K. (2020) · eDiss (Georg-August-Universität Göttingen) · doi:10.53846/goediss-8016
Inflammation and accumulating risk for developing psychiatric disorders
Money, K. M. (2016)
Ghosh, S., Shaftel, S. S., Kyrkanides, S., Olschowka, J. A., & O’Banion, M. K. (2021) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2021.02.10.430570
Self-citationMalm, T., Magga, J. M., & Koıstınaho, J. (2012) · Current Translational Geriatrics and Experimental Gerontology Reports · doi:10.1007/s13670-012-0008-3
Sustained IL-1β overexpression reduces amyloid pathology in a mouse model of AD
(2007) · Nature Clinical Practice Neurology · doi:10.1038/ncpneuro0573
(2007) · Nature Reviews Drug Discovery · doi:10.1038/nrd2391
Alzheimer disease and neuroinflammation in Down syndrome
Ganguly, B. B. (2022) · Elsevier eBooks · doi:10.1016/b978-0-323-90456-8.00014-4
Kokhan, V. S., Nesterov, M. S., & Levashova, A. I. (2023) · Доклады Российской академии наук Науки о жизни · doi:10.31857/s2686738923600139
Metadata
- Authors
- Shaftel, S. S., Kyrkanides, S., Olschowka, J. A., Miller, J.-N. H., Johnson, R. E., & O’Banion, M. K.
- Affiliations
- University of Rochester Medicine (US)
- Corresponding author
- O’Banion, M. Kerry
- Venue
- Journal of Clinical Investigation
- Published
- 2007-06-01
- Volume
- 117
- Issue
- 6
- Pages
- 1595-1604
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1878531
- OpenAlex
- W2105385589
- Cited by
- 433
- References
- 46
- Citations by year
- 2026: 8 · 2025: 25 · 2024: 16 · 2023: 18 · 2022: 34 · 2021: 22 · 2020: 20 · 2019: 26 · 2018: 23 · 2017: 20 · 2016: 18 · 2015: 24 · 2014: 32 · 2013: 26 · 2012: 35
- FWCI
- 12.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Rochester
- National Institutes of Health (14642)
- Medical Center, University of Rochester
- National Institute of General Medical Sciences (GM 07356, T32GM007356)
- National Institute of Neurological Disorders and Stroke (NS048522, R29NS033553, NS 33553, R21NS048522, R01NS033553)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- IL-1β, neuroinflammation, Alzheimer's disease, amyloid plaques, hippocampus, astrocyte activation, microglial activation, inflammatory cytokines, APPswe/PS1dE9 transgenic mice, amyloid-beta
- MeSH terms
- Alzheimer Disease, Animals, Base Sequence, Disease Models, Animal, Hippocampus, Humans, Inflammation, Mice, Transgenic, Nerve Degeneration, Recombinant Proteins, Gene Expression, Amyloid beta-Protein Precursor, DNA Primers, Mice, Interleukin-1beta, Presenilin-1, 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 ›
Are you an author, or do you see a problem with this page? Request a review
