The DOI matches its Crossref record; 32 of the 34 references it cites were found in a registry or an index.
NLRP3 is activated in Alzheimer’s disease and contributes to pathology in APP/PS1 mice
Open accessAbstract
Alzheimer’s disease is the world’s most common dementing illness. Deposition of amyloid-β peptide drives cerebral neuroinflammation by activating microglia. Indeed, amyloid-β activation of the NLRP3 inflammasome in microglia is fundamental for interleukin-1β maturation and subsequent inflammatory events. However, it remains unknown whether NLRP3 activation contributes to Alzheimer’s disease in vivo. Here we demonstrate strongly enhanced active caspase-1 expression in human mild cognitive impairment and brains with Alzheimer’s disease, suggesting a role for the inflammasome in this neurodegenerative disease. Nlrp3−/− or Casp1−/− mice carrying mutations associated with familial Alzheimer’s disease were largely protected from loss of spatial memory and other sequelae associated with Alzheimer’s disease, and demonstrated reduced brain caspase-1 and interleukin-1β activation as well as enhanced amyloid-β clearance. Furthermore, NLRP3 inflammasome deficiency skewed microglial cells to an M2 phenotype and resulted in the decreased deposition of amyloid-β in the APP/PS1 model of Alzheimer’s disease. These results show an important role for the NLRP3/caspase-1 axis in the pathogenesis of Alzheimer’s disease, and suggest that NLRP3 inflammasome inhibition represents a new therapeutic intervention for the 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
“Rat research has identified the NLRP3-ASC inflammasome as a major mechanism through which microglia may drive pathological features of AD [92,93,94].”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [92]
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
“Both beta-amyloids and tau can activate the NLRP3-ASC inflammasome within microglia [92,93].”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [92]
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
“The nucleotide-binding oligomerization domain-like receptor, pyrin domain-containing 3 (NLRP3), within microglia recruits the adaptor protein apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC) to form an inflammasome complex.”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [92]
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
“ITGAM/CD11b (or CR3A), is a cell surface receptor involved in activation, migration and phagocytosis of immune cells, so much so that ITGAM/CD11b is used as a marker of activated microglia (Matsuoka et al., 2001; Heneka et al., 2013; Kamphuis et al., 2016).”
From Genetic variability in response to amyloid beta deposition influences Alzheimer’s disease risk (2019) · cites this paper as Heneka et al., 2013
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
“In APP/PS1 mice model, NLRP3 knockout reduced Aβ deposition by enhancing phagocytic clearance capacity and increasing extracellular Aβ degradation by insulin- degrading enzyme (IDE).354”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [354]
Experimental — accuracy not yet measured
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
“The activation of hippocampal NLRP3 inflammasome-mediated pyroptosis is associated with neuronal damage, cognitive decline, and neuronal death (Hanslik & Ulland, 2020; Heneka et al., 2013; Ising et al., 2019; Venegas et al., 2017).”
From Picroside II Alleviates the Progression of Alzheimer’s Disease via the NLRP3/Caspase-1/GSDMD Pathway (2025) · cites this paper as Heneka et al., 2013
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
“NLRP3 or caspase-1 knockdown in AD mouse models has yielded promising results in decreasing Aβ accumulation, improving spatial memory, and alleviating other AD-related symptoms (Heneka et al., 2013).”
From Picroside II Alleviates the Progression of Alzheimer’s Disease via the NLRP3/Caspase-1/GSDMD Pathway (2025) · cites this paper as Heneka et al., 2013
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
“Ablation of Nlrp3 or Casp1 in APP/PS1 mice rescued spatial memory and behavioral deficits, LTP suppression and spine loss observed in these mice [77].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [77]
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
“However, another study reported strongly increased levels of active caspase-1 in early-onset AD and LOAD patients as well as in MCI individuals [77].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [77]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“This inflammasome complex is responsible for the production of IL-1 beta, which is a proinflammatory cytokine.”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [92]
The cited source says what the claim attributes to it.
In the citing paper
“IL-1 beta was shown to exacerbate tau pathologies [97] and reduce microglial phagocytic activity [92,93,94].”
From The Role of Cortisol in Chronic Stress, Neurodegenerative Diseases, and Psychological Disorders (2023) · cites this paper as [92]
The cited source says what the claim attributes to it.
In the citing paper
“Furthermore, microglial function may also be of relevance to cognitive performance, as suggested by recent experimental data, which showed that improved microglial clearance was protective in terms of memory function (17).”
From SUCLG2 identified as both a determinator of CSF Aβ1–42 levels and an attenuator of cognitive decline in Alzheimer's disease (2014) · cites this paper as [17]
The cited source says what the claim attributes to it.
In the citing paper
“Proinflammatory environments and signalling are a prominent observation in AD brain pathology [39].”
From Heterozygous expression of the Alzheimer’s disease-protective PLCγ2 P522R variant enhances Aβ clearance while preserving synapses (2022) · cites this paper as [39]
The cited source says what the claim attributes to it.
In the citing paper
“Inhibiting or downregulating the NLRP3 inflammasome ameliorates AD neuropathology in animal models, which opens up a therapeutic avenue for modulators of NLRP3 activation in AD.”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [77]
The cited source says what the claim attributes to it.
In the citing paper
“APP/PS1/Nlrp3−/− and APP/PS1/Casp1−/− mice also displayed decreased Aβ plaque deposition, suggesting that NLRP3 inflammasome activation impairs microglial capacity to clear Aβ [77].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [77]
The cited source says what the claim attributes to it.
In the citing paper
“APP/PS1/Nlrp3−/− and APP/PS1/Casp1−/− mice also displayed decreased Aβ plaque deposition, suggesting that NLRP3 inflammasome activation impairs microglial capacity to clear Aβ [77].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [77]
The cited source says what the claim attributes to it.
In the citing paper
“The decreased plaque deposition was also related to increased levels of the proteolytic enzyme insulin-degrading enzyme (IDE) [77], previously reported to degrade Aβ [83].”
From Microglial function, INPP5D/SHIP1 signaling, and NLRP3 inflammasome activation: implications for Alzheimer’s disease (2023) · cites this paper as [77]
The cited source says what the claim attributes to it.
In the citing paper
“NLRP3 deficiency reduces amyloid deposition and rescues memory deficits in the APP/PS1 model of AD [18].”
From 25-Hydroxycholesterol amplifies microglial IL-1β production in an apoE isoform-dependent manner (2020) · cites this paper as [18]
In the citing paper
“One of the key biological functions of CASP1 is the cleavage of prointerleukin-1β (IL-1β) into the mature biological active cytokine, which is largely overexpressed in brains of patients with AD.44”
From APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease (2016) · cites this paper as [44]
In the citing paper
“Preclinical studies support the concept that CASP1-directed increase of IL-1β can augment the deposition of β-amyloid within the brain to worsen Alzheimer's symptoms.44”
From APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease (2016) · cites this paper as [44]
In the citing paper
“CASP1, an essential component of NLPR3 inflammasomes, encodes a cysteine protease that is largely overexpressed in brains of patients with AD.44”
From APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease (2016) · cites this paper as [44]
In the citing paper
“Notably, Aβ also can activate NF-κB signaling and the NLRP3-ASC inflammasome [426, 427], suggesting that Aβ and tau share common mechanisms in microglia activation.”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [427]
In the citing paper
“The NLRP3 inflammasome is critical for maturation of IL-1β, and loss of NLRP3 in APP/PS1 decreased amyloid burden (131).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [131]
In the citing paper
“Microglia express multiple receptors that can bind Aβ and trigger inflammation, such as CD36 (105), TLR2, TLR4, TLR6 (17), and NLRP3 (106)”
From Microglia Function in the Central Nervous System During Health and Neurodegeneration (2017) · cites this paper as [106]
In the citing paper
“NLRP3 and caspase-1 genetic deletion results in decreased Aβ deposition, reduced IL-1β release from microglia and improved cognitive performance in APPPS1 mice (Heneka et al., 2013).”
From Alzheimer Disease: An Update on Pathobiology and Treatment Strategies (2019) · cites this paper as Heneka et al., 2013
In the citing paper
“Toll-like receptors and NOD-like receptors have been previously implicated in the microglia response to Aβ accumulation and shown to mediate an inflammatory response that contributes to pathology”
From TREM2 Maintains Microglial Metabolic Fitness in Alzheimer’s Disease (2017) · cites this paper as Heneka et al., 2013
In the citing paper
“Animal studies confirmed this significant involvement of NLRP activation, as APP/PS1 mice, lacking the expression of ASC, caspase-1, or NLRP3 had significantly reduced hippocampal and cortical amyloid plaque deposition and ameliorated disease outcome (229, 230).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [230]
In the citing paper
“Recently, an alternative pathway has been described for intracellular signaling produced by the binding of Aβ to microglial cells, activating NLRP3 inflammasome (Heneka et al., 2013; Sheedy et al., 2013).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Heneka et al., 2013
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
A synaptic model of memory: long-term potentiation in the hippocampus
Bliss, T. V. P., & Collingridge, G. L. (1993) · Nature · doi:10.1038/361031a0 · Cited by 11,566
The NALP3 inflammasome is involved in the innate immune response to amyloid-β
Halle, A., Hornung, V., Petzold, G. C., Stewart, C. R., Monks, B. G., Reinheckel, T., Fitzgerald, K. A., Latz, E., Moore, K. J., & Golenbock, D. T. (2008) · Nature Immunology · doi:10.1038/ni.1636 · Cited by 2,441
Self-citationThe Inflammasomes: Guardians of the Body
Martinon, F., Mayor, A., & Tschopp, J. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132715 · Cited by 2,436
Decreased Clearance of CNS β-Amyloid in Alzheimer’s Disease
Mawuenyega, K. G., Sigurdson, W., Ovod, V., Munsell, L., Kasten, T., Morris, J. C., Yarasheski, K. E., & Bateman, R. J. (2010) · Science · doi:10.1126/science.1197623 · Cited by 2,078
Li, P., Allen, H., Banerjee, S., Franklin, S., Herzog, L., Johnston, C. G., McDowell, J., Paskind, M. P., Rodman, L., Salfeld, J. G., et al. (1995) · Cell · doi:10.1016/0092-8674(95)90490-5 · Cited by 1,408
Microglial Dysfunction and Defective β-Amyloid Clearance Pathways in Aging Alzheimer's Disease Mice
Hickman, S. E., Allison, E. K., & El Khoury, J. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.0616-08.2008 · Cited by 1,329 · cited 1×
“Cytokines, including IL-1 β , were found to impair microglial clearance functions 16,17 .”
Bevins, R. A., & Besheer, J. (2006) · Nature Protocols · doi:10.1038/nprot.2006.205 · Cited by 1,278
Bacterial RNA and small antiviral compounds activate caspase-1 through cryopyrin/Nalp3
Kanneganti, T., Özören, N., Body–Malapel, M., Amer, A. O., Park, J., Franchi, L., Whitfield, J. R., Barchet, W., Colonna, M., Vandenabeele, P., et al. (2006) · Nature · doi:10.1038/nature04517 · Cited by 1,149
Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice
Chapman, P. F., White, G. L., Jones, M. W., Cooper-Blacketer, D., Marshall, V. J., Irizarry, M., Younkin, L., Good, M. A., Bliss, T. V. P., Hyman, B. T., et al. (1999) · Nature Neuroscience · doi:10.1038/6374 · Cited by 946
El Khoury, J., Toft, M., Hickman, S. E., Means, T. K., Terada, K., Geula, C., & Luster, A. D. (2007) · Nature Medicine · doi:10.1038/nm1555 · Cited by 915
Cited by
Sorted by citations
Items 901–1,000 of 1,031
Elongator mutation in mice induces neurodegeneration and ataxia-like behavior
Kojic, M., Gaik, M., Kiska, B., Salerno-Kochan, A., Hunt, S., Tedoldi, A., Mureev, S., Jones, A., Whittle, B., Genovesi, L. A., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-05765-6 · Cited by 56
Scarabino, D., Peconi, M., Broggio, E., Gambina, G., Maggi, E., Armeli, F., Mantuano, E., Morello, M., Corbo, R. M., & Businaro, R. (2020) · Experimental Gerontology · doi:10.1016/j.exger.2020.110945 · Cited by 59
Exercise-Induced Modulation of Neuroinflammation in Models of Alzheimer’s Disease
Kelly, Á. M. (2018) · Brain Plasticity · doi:10.3233/bpl-180074 · Cited by 55
Microglial Immunometabolism in Alzheimer’s Disease
Shippy, D. C., & Ulland, T. K. (2020) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2020.563446 · Cited by 56
Cosker, K., Mallach, A., Limaye, J., Piers, T. M., Staddon, J. M., Neame, S. J., Hardy, J., & Pocock, J. M. (2021) · Scientific Reports · doi:10.1038/s41598-021-91207-1 · Cited by 53
Directly targeting ASC by lonidamine alleviates inflammasome-driven diseases
Chen, C., Zhou, Y., Ning, X., Li, S., Xue, D., Wei, C., Zhu, Z., Sheng, L., Lu, B., Li, Y., et al. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02682-w · Cited by 59
The Relationship between NALP3 and Autoinflammatory Syndromes
Campbell, L., Raheem, I., Malemud, C. J., & Askari, A. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17050725 · Cited by 55
What do we know about the inflammasome in humans?
Amin, J., Boche, D., & Rakić, S. (2016) · Brain Pathology · doi:10.1111/bpa.12479 · Cited by 56
Ding, Q., Shen, L., Nie, X., Lü, B., Pan, X., Su, Z., Yan, A., Yan, R., Zhou, Y., Li, L., et al. (2018) · Pathology - Research and Practice · doi:10.1016/j.prp.2018.05.012 · Cited by 55
Garcez, M. L., Mina, F., Bellettini‐Santos, T., da Luz, A. P., Schiavo, G. L., Macieski, J. M. C., Medeiros, E. B., Marques, A. O., Magnus, N. Q., & Budni, J. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-1211-9 · Cited by 54
Park, M. H., Lee, M., Nam, G., Kim, M., Kang, J., Choi, B. J., Jeong, M. S., Park, K. H., Han, W. H., Tak, E., et al. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1916318116 · Cited by 54
Enduring Changes in Neuronal Function upon Systemic Inflammation Are NLRP3 Inflammasome Dependent
Beyer, M. M. S., Lonnemann, N., Remus, A., Latz, E., Heneka, M. T., & Korte, M. (2020) · The Journal of Neuroscience · doi:10.1523/jneurosci.0200-20.2020 · Cited by 55
Self-citationγ-Secretase and its modulators: Twenty years and beyond
Xia, W. (2019) · Neuroscience Letters · doi:10.1016/j.neulet.2019.02.011 · Cited by 54
Li, Y., Xu, P., Shan, J., Sun, W., Ji, X., Chi, T., Liu, P., & Zou, L. (2019) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2019.109618 · Cited by 52
Chronic cerebral hypoperfusion activates AIM2 and NLRP3 inflammasome
Matsuyama, H., Shindo, A., Shimada, T., Yata, K., Wakita, H., Takahashi, R., & Tomimoto, H. (2020) · Brain Research · doi:10.1016/j.brainres.2020.146779 · Cited by 53
McCarty, M. F., Assanga, S. B. I., Luján, L. M. L., O’Keefe, J. H., & DiNicolantonio, J. J. (2020) · Nutrients · doi:10.3390/nu13010047 · Cited by 55
An Epigenetic Insight into NLRP3 Inflammasome Activation in Inflammation-Related Processes
Raneros, A. B., Bernet, C. R., Flórez, A. B., & Suárez-Álvarez, B. (2021) · Biomedicines · doi:10.3390/biomedicines9111614 · Cited by 53
Targeting MicroRNA-485-3p Blocks Alzheimer’s Disease Progression
Koh, H., Lee, S., Lee, H., Min, J.-W., Iwatsubo, T., Teunissen, C. E., Cho, H., & Ryu, J. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222313136 · Cited by 58
Immune cell dynamics in the CNS: Learning from the zebrafish
Oosterhof, N., Boddeke, E., & van Ham, T. J. (2014) · Glia · doi:10.1002/glia.22780 · Cited by 53
Neural stem/progenitor cells in Alzheimer's disease.
Tincer, G., Mashkaryan, V., Bhattarai, P., & Kızıl, Ç. (2016) · Europe PMC (PubMed Central) · Cited by 56
AIM 2 inflammasomes regulate neuronal morphology and influence anxiety and memory in mice
Wu, P.-J., Liu, H., Huang, T., & Hsueh, Y. (2016) · Scientific Reports · doi:10.1038/srep32405 · Cited by 56
Silymarin’s Inhibition and Treatment Effects for Alzheimer’s Disease
Guo, H. W., Cao, H., Cui, X., Zheng, W., Wang, S., Yu, J., & Chen, Z. (2019) · Molecules · doi:10.3390/molecules24091748 · Cited by 54
Li, L., Wu, X., Zhao, X.-J., Xu, L., Pan, C., & Zhang, Z. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01744-1 · Cited by 56
Shang, D., Hong, Y., Xie, W., Tu, Z., & Xu, J. L. (2020) · Frontiers in Neurology · doi:10.3389/fneur.2020.00929 · Cited by 54
Israelov, H., Ravid, O., Atrakchi, D., Rand, D., Goldman, S. E., Bresler, Y., Twitto‐Greenberg, R., Omesi, L., Zaltsman, S. L., Gosselet, F., et al. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01927-w · Cited by 53
The role of NLRP3 in lead-induced neuroinflammation and possible underlying mechanism
Su, P., Wang, D., Cao, Z., Chen, J., & Zhang, J. (2021) · Environmental Pollution · doi:10.1016/j.envpol.2021.117520 · Cited by 53
Panda, C., Voelz, C., Habib, P., Mevissen, C., Pufe, T., Beyer, C., Gupta, S. K., & Slowik, A. (2021) · Cells · doi:10.3390/cells10071652 · Cited by 54
Inflammation: major denominator of obesity, Type 2 diabetes and Alzheimer’s disease-like pathology?
Kacířová, M., Zmeškalová, A., Kořínková, L., Železná, B., Kuneš, J., & Maletı́nská, L. (2020) · Clinical Science · doi:10.1042/cs20191313 · Cited by 56
Synaptic elimination by microglia and disturbed higher brain functions
Miyanishi, K., Sato, A., Kihara, N., Utsunomiya, R., & Tanaka, J. (2020) · Neurochemistry International · doi:10.1016/j.neuint.2020.104901 · Cited by 53
Nakanishi, K., Sakakima, H., Norimatsu, K., Otsuka, S., Takada, S., Tani, A., & Kikuchi, K. (2020) · Experimental Neurology · doi:10.1016/j.expneurol.2020.113590 · Cited by 53
Aging-Dependent Mitophagy Dysfunction in Alzheimer’s Disease
Song, M., Zhao, X., & Song, F. (2021) · Molecular Neurobiology · doi:10.1007/s12035-020-02248-y · Cited by 59
Vitamin K2 Holds Promise for Alzheimer’s Prevention and Treatment
Popescu, A., & German, M. (2021) · Nutrients · doi:10.3390/nu13072206 · Cited by 57
The role of Cl− and K+ efflux in NLRP3 inflammasome and innate immune response activation
Koumangoye, R. B. (2022) · American Journal of Physiology-Cell Physiology · doi:10.1152/ajpcell.00421.2021 · Cited by 55
Wang, S.-Y., Fu, X., Duan, R., Wei, B., Cao, H., Yan, E., Chen, S., Zhang, Y.-D., & Jiang, T. (2022) · Neural Regeneration Research · doi:10.4103/1673-5374.346468 · Cited by 53
Zhou, X., Qiu, W., Yu, L., Pan, R., Teng, J., Sang, Z., Law, B. Y. K., Zhao, Y., Zhang, L., Yan, L., et al. (2022) · Inflammation and Regeneration · doi:10.1186/s41232-022-00209-7 · Cited by 54
Links between COVID-19 and Alzheimer’s Disease—What Do We Already Know?
Rudnicka-Drożak, E., Drożak, P., Mizerski, G., Zaborowski, T., Ślusarska, B. J., Nowicki, G., & Drożak, M. (2023) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph20032146 · Cited by 57
Tang, L., Liu, S., Li, S., Chen, Y., Xie, B., & Zhou, J. F. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms241210127 · Cited by 57
Microglial activation as a hallmark of neuroinflammation in Alzheimer’s disease
Ebrahimi, R., Nejad, S. S., Tafti, M. F., Karimi, Z., Sadr, S. R., Hussein, D. R., Talebian, N., & Esmaeilpour, K. (2025) · Metabolic Brain Disease · doi:10.1007/s11011-025-01631-9 · Cited by 58
Inflammasome Activation in Chronic Glomerular Diseases
Conley, S. M., Abais, J. M., Boini, K. M., & Li, P. (2016) · Current Drug Targets · doi:10.2174/1389450117666160817103435 · Cited by 53
Effects of COX1-2/5-LOX blockade in Alzheimer transgenic 3xTg-AD mice
Bitto, A., Giuliani, D., Pallio, G., Irrera, N., Vandini, E., Canalini, F., Zaffe, D., Ottani, A., Minutoli, L., Rinaldi, M., et al. (2017) · Inflammation Research · doi:10.1007/s00011-017-1022-x · Cited by 53
Jiang, L., Li, X., Mortadza, S. A. S., Lovatt, M., & Yang, W. (2018) · Ageing Research Reviews · doi:10.1016/j.arr.2018.07.002 · Cited by 53
N-AS-triggered SPMs are direct regulators of microglia in a model of Alzheimer’s disease
Lee, J. Y., Han, S. H., Park, M. H., Song, I., Choi, M., Yu, E., Park, C., Kim, H.-J., Kim, S. H., Schuchman, E. H., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-16080-4 · Cited by 53
Alzheimer’s Disease: A Molecular View of β-Amyloid Induced Morbific Events
Asik, R. M., Suganthy, N., Aarifa, M. A., Kumar, A., Szigeti, K., Máthé, D., Gulyás, B. Z., Archunan, G., & Padmanabhan, P. (2021) · Biomedicines · doi:10.3390/biomedicines9091126 · Cited by 54
The AIM2 inflammasome is activated in astrocytes during the late phase of EAE
Barclay, W. E., Deerhake, M. E., Inoue, M., Nonaka, T., Nozaki, K., Luzum, N. A., Aggarwal, N., Miao, E. A., & Shinohara, M. L. (2022) · JCI Insight · doi:10.1172/jci.insight.155563 · Cited by 55
Zheng, Y., Zhang, X., Zhang, R., Wang, Z., Gan, J., Gao, Q., Yang, L., Xu, P., & Jiang, X. (2023) · International Journal of Molecular Medicine · doi:10.3892/ijmm.2023.5314 · Cited by 52
Iron potentiates microglial interleukin‐1β secretion induced by amyloid‐β
Nnah, I. C., Lee, C., & Wessling‐Resnick, M. (2019) · Journal of Neurochemistry · doi:10.1111/jnc.14906 · Cited by 54
14,15-Epoxyeicosatrienoic Acid Alleviates Pathology in a Mouse Model of Alzheimer's Disease
Chen, W., Wang, M., Zhu, M., Xiong, W., Qin, X., & Zhu, X. (2020) · Journal of Neuroscience · doi:10.1523/jneurosci.1246-20.2020 · Cited by 52
Entrectinib inhibits NLRP3 inflammasome and inflammatory diseases by directly targeting NEK7
Jin, X., Liu, D., Zhou, X., Luo, X., Huang, Q., & Huang, Y. (2023) · Cell Reports Medicine · doi:10.1016/j.xcrm.2023.101310 · Cited by 53
The Microtubule-associated Protein EB1 Links AIM2 Inflammasomes with Autophagy-dependent Secretion
Wang, L., Huang, H., Huang, M.-P., Liou, W., Chang, Y., Wu, C., Ojcius, D. M., & Chang, Y. (2014) · Journal of Biological Chemistry · doi:10.1074/jbc.m114.559153 · Cited by 54
Microglia in Neurodegenerative Disorders
Tejera, D., & Heneka, M. T. (2019) · Methods in molecular biology · doi:10.1007/978-1-4939-9658-2_5 · Cited by 54
Self-citationWang, C., Zhang, Q., Xun, Z., Yuan, L., Li, R., Li, X., Tian, S.-Y., Xin, N., & Xu, Y. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101672 · Cited by 52
Myricetin as a Promising Molecule for the Treatment of Post-Ischemic Brain Neurodegeneration
Pluta, R. M., Januszewski, S., & Czuczwar, S. J. (2021) · Nutrients · doi:10.3390/nu13020342 · Cited by 49
Cytokine signaling convergence regulates the microglial state transition in Alzheimer’s disease
Lau, S., Fu, A. K. Y., & Ip, N. Y. (2021) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-021-03810-0 · Cited by 55
BAD-mediated neuronal apoptosis and neuroinflammation contribute to Alzheimer's disease pathology
Zhang, L., Qian, Y., Li, J., Zhou, X., Xu, H. J., Yan, J., Xiang, J., Yuan, X., Sun, B., Sisodia, S. S., et al. (2021) · iScience · doi:10.1016/j.isci.2021.102942 · Cited by 54
Tian, D., Xing, Y., Gao, W., Zhang, H., Song, Y., Tian, Y., & Dai, Z. (2022) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2021.801422 · Cited by 52
Calcium-Sensing Receptors of Human Neural Cells Play Crucial Roles in Alzheimer's Disease
Chiarini, A., Armato, U., Liu, D., & Dal Prà, I. (2016) · Frontiers in Physiology · doi:10.3389/fphys.2016.00134 · Cited by 51
León, B. E., Kang, S., Franca-Solomon, G., Shang, P., & Choi, D. (2022) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2021.778456 · Cited by 56
Microglial TLR4/NLRP3 Inflammasome Signaling in Alzheimer’s Disease
Li, Y., Chen, X., Zhou, M., Feng, S., Peng, X., & Wang, Y. (2023) · Journal of Alzheimer s Disease · doi:10.3233/jad-230273 · Cited by 58
Tau induces inflammasome activation and microgliosis through acetylating NLRP3
Zhang, L., Gai, Y., Liu, Y., Meng, D., Zeng, Y., Luo, Y., Zhang, H., Wang, Z., Yang, M., Li, Y., et al. (2024) · Clinical and Translational Medicine · doi:10.1002/ctm2.1623 · Cited by 52
Synergistic Actions of Microglia and Astrocytes in the Progression of Alzheimer's Disease
Bouvier, D. S., & Murai, K. K. (2015) · Journal of Alzheimer s Disease · doi:10.3233/jad-143156 · Cited by 52
Kawahara, K., Suenobu, M., Ohtsuka, H., Kuniyasu, A., Sugimoto, Y., Nakagomi, M., Fukasawa, H., Shudo, K., & Nakayama, H. (2014) · Journal of Alzheimer's Disease · doi:10.3233/jad-132720 · Cited by 51
Cao, X., Xu, H., Feng, W., Su, D., & Xiao, M. (2018) · Brain Research Bulletin · doi:10.1016/j.brainresbull.2018.10.007 · Cited by 52
Kodidela, S., Gerth, K. A., Haque, S., Gong, Y., Ismael, S., Singh, A. K., Ishrat, T., & Kumar, S. (2019) · Cells · doi:10.3390/cells8090968 · Cited by 51
Pan, H., Qiu, H., Zhang, K., Zhang, P., Liang, W., Yang, M., Mou, C., Lin, M., He, M., Xiao, X., et al. (2019) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.9b00503 · Cited by 53
Tian, H., Li, G., Xu, G., Liu, J., Wan, X., Zhang, J., Xie, S., Cheng, J. R., & Gao, S. (2020) · European Archives of Psychiatry and Clinical Neuroscience · doi:10.1007/s00406-020-01128-9 · Cited by 52
Modeling the Interaction between the Microenvironment and Tumor Cells in Brain Tumors
Pasqualini, C., Kozaki, T., Bruschi, M., Nguyen, T. H. H., Minard‐Colin, V., Castel, D., Grill, J., & Ginhoux, F. (2020) · Neuron · doi:10.1016/j.neuron.2020.09.018 · Cited by 55
Therapeutic Role of Inflammasome Inhibitors in Neurodegenerative Disorders
Lahooti, B., Chhibber, T., Bagchi, S., Varahachalam, S. P., & Jayant, R. D. (2021) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2020.11.004 · Cited by 50
Pike, A. F., Szabó, I., Veerhuis, R., & Bubacco, L. (2022) · npj Parkinson s Disease · doi:10.1038/s41531-022-00293-z · Cited by 50
Inflammasome Activation in Parkinson’s Disease
Jewell, S. L., Herath, A. M., & Gordon, R. (2022) · Journal of Parkinson s Disease · doi:10.3233/jpd-223338 · Cited by 53
Eitas, T. K., Chou, W.-C., Wen, H., Gris, D., Robbins, G. R., Brickey, W. J., Oyama, Y., & Ting, J. P. ‐. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m113.533034 · Cited by 51
Nitric Oxide Sensors for Biological Applications
Iverson, N. M., Hofferber, E. M., & Stapleton, J. (2018) · Chemosensors · doi:10.3390/chemosensors6010008 · Cited by 51
Herrera, M. G., Pizzuto, M., Lonez, C., Rott, K., Hütten, A., Sewald, N., Ruysschaert, J., & Dodero, V. I. (2018) · Nanomedicine Nanotechnology Biology and Medicine · doi:10.1016/j.nano.2018.04.014 · Cited by 51
Schmöle, A., Lundt, R., Toporowski, G., Hansen, J. N., Beins, E. C., Halle, A., & Zimmer, A. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180230 · Cited by 51
Self-citationThe role of NLRP3 inflammasome in stroke and central poststroke pain
Li, S., Zhang, Y., Ma, S., Yi, Y., Yu, H., Pei, L., & Feng, D. (2018) · Medicine · doi:10.1097/md.0000000000011861 · Cited by 50
Nasoohi, S., Parveen, K., & Ishrat, T. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180735 · Cited by 51
Wang, Y., Guan, X., Chen, X., Cai, Y., Ma, Y., Ma, J., Zhang, Q., Dai, L., Fan, X., & Bai, Y. (2019) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201801407 · Cited by 47
The NLRP3 inflammasome: a new player in neurological diseases
Eren, E., & Özören, N. (2019) · TURKISH JOURNAL OF BIOLOGY · doi:10.3906/biy-1909-31 · Cited by 54
Role of the NLRP3 inflammasome in neurodegenerative diseases and therapeutic implications
Duan, Y., Kelley, N., & He, Y. (2020) · Neural Regeneration Research · doi:10.4103/1673-5374.272576 · Cited by 50
Molecular Mechanism of Apoptosis by Amyloid β-Protein Fibrils Formed on Neuronal Cells
Takada, E., Okubo, K., Yano, Y., Iida, K., Someda, M., Hirasawa, A., Yonehara, S., & Matsuzaki, K. (2020) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.0c00011 · Cited by 50
Ellagic Acid Protects Dopamine Neurons via Inhibition of NLRP3 Inflammasome Activation in Microglia
He, X., Zhou, Y.-Z., Sheng, S., Li, J., Wang, G., & Zhang, F. (2020) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2020/2963540 · Cited by 50
P2X7-deficiency improves plasticity and cognitive abilities in a mouse model of Tauopathy
Carvalho, K., Martin, E., Cès, A., Sarrazin, N., Lagouge-Roussey, P., Nous, C., Boucherit, L., Youssef, I., Prigent, A., Faivre, É., et al. (2021) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2021.102139 · Cited by 54
Novel insights into RIPK1 as a promising target for future Alzheimer’s disease treatment
Li, S., Qu, L., Wang, X., & Kong, L. (2021) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2021.107979 · Cited by 51
Regulation of microglial physiology by the microbiota
Cook, J., & Prinz, M. (2022) · Gut Microbes · doi:10.1080/19490976.2022.2125739 · Cited by 49
Pleiotropic Roles of P2X7 in the Central Nervous System
Kanellopoulos, J. M., & Delarasse, C. (2019) · Frontiers in Cellular Neuroscience · doi:10.3389/fncel.2019.00401 · Cited by 48
Ramirez, A., van der Flier, W. M., Herold, C., Ramonet, D., Heilmann, S., Lewczuk, P., Popp, J., Lacour, A., Drichel, D., Louwersheimer, E., et al. (2014) · Human Molecular Genetics · doi:10.1093/hmg/ddu372 · Cited by 49
Self-citationUnconventional Pathways of Secretion Contribute to Inflammation
Daniels, M. J. D., & Brough, D. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms18010102 · Cited by 50
The Post-amyloid Era in Alzheimer's Disease: Trust Your Gut Feeling
Osorio, C. P., Kanukuntla, T., Diaz, E. L., Jafri, N., Cummings, M., & Sfera, A. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00143 · Cited by 50
Dolatshahi, M., Sabahi, M., & Aarabi, M. H. (2021) · Molecular Neurobiology · doi:10.1007/s12035-020-02236-2 · Cited by 51
Beta-Hydroxybutyrate, Friend or Foe for Stressed Hearts
Chu, Y., Zhang, C., & Xie, M. (2021) · Frontiers in Aging · doi:10.3389/fragi.2021.681513 · Cited by 52
Zhang, T., Ding, S., & Wang, R. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms221910866 · Cited by 53
Abdallah, I. M., Al-Shami, K. M., Yang, E., Wang, J., Guillaume, C., & Kaddoumi, A. (2022) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.2c00005 · Cited by 52
Hallmarks of neurodegenerative disease: A systems pharmacology perspective
Bloomingdale, P., Karelina, T., Ramakrishnan, V., Bakshi, S., Véronneau‐Veilleux, F., Moye, M., Sekiguchi, K., Meno‐Tetang, G. M. L., Mohan, A., Maithreye, R., et al. (2022) · CPT Pharmacometrics & Systems Pharmacology · doi:10.1002/psp4.12852 · Cited by 54
Relationships between Inflammation and Age-Related Neurocognitive Changes
Jin, R., Chan, A. K. Y., Wu, J., & Lee, T. M. C. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232012573 · Cited by 54
Fan, M., Wang, C., Zhao, X., Jiang, Y. Z., & Wang, C. (2023) · International Immunopharmacology · doi:10.1016/j.intimp.2023.110287 · Cited by 51
Yang, S., Li, M., Lian, G., Wu, Y., Cui, J., & Wang, L. (2024) · Autophagy · doi:10.1080/15548627.2024.2395158 · Cited by 49
Zhang, Z., Li, M., Li, X., Feng, Z., Luo, G., Wang, Y., & Gao, X. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03254-w · Cited by 56
Wang, H., Xia, H., Bai, J., Wang, Z., Wang, Y., Lin, J., Cheng, C., Chen, W., Zhang, J., Zhang, Q., et al. (2025) · Journal of Hazardous Materials · doi:10.1016/j.jhazmat.2025.137310 · Cited by 54
Bioenergetic Dysfunction and Inflammation in Alzheimer’s Disease: A Possible Connection
Wilkins, H., Carl, S. M., Greenlief, A. C. S., Festoff, B. W., & Swerdlow, R. H. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00311 · Cited by 51
CCL17 exerts a neuroimmune modulatory function and is expressed in hippocampal neurons
Fülle, L., Offermann, N., Hansen, J. N., Breithausen, B., Erazo, A. B., Schanz, O., Radau, L., Gondorf, F., Knöpper, K., Alferink, J., et al. (2018) · Glia · doi:10.1002/glia.23507 · Cited by 52
Self-citationMcFarland, K. N., & Chakrabarty, P. (2022) · Neurotherapeutics · doi:10.1007/s13311-021-01179-3 · Cited by 48
Metadata
- Authors
- Heneka, M. T., Kummer, M. P., Stutz, A., Delekate, A., Schwartz, S., Vieira-Saecker, A., Griep, A., Axt, D., Remus, A., Tzeng, T.-C., Gelpi, E., Halle, A., Korte, M., Latz, E., & Golenbock, D. T.
- Affiliations
- University of Bonn (DE)
- Technische Universität Braunschweig (DE)
- University of Massachusetts Chan Medical School (US)
- Center of Advanced European Studies and Research (DE)
- Corresponding author
- Heneka, Michael T.
- Latz, Eicke
- Golenbock, Douglas T.
- ORCID
- Venue
- Nature
- Published
- 2012-12-19
- Volume
- 493
- Issue
- 7434
- Pages
- 674-678
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- PMC
- PMC3812809
- OpenAlex
- W1993976394
- Semantic Scholar
- 3a962c33176c94bc0dd8bfea4ebe2eb83be8a01e
- Cited by
- 2,898
- References
- 34
- Citations by year
- 2026: 274 · 2025: 270 · 2024: 273 · 2023: 270 · 2022: 306 · 2021: 314 · 2020: 261 · 2019: 203 · 2018: 187 · 2017: 147 · 2016: 117 · 2015: 112 · 2014: 99 · 2013: 62
- FWCI
- 35.07
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Open Repository and Bibliography (University of Luxembourg) (submittedVersion, other-oa)
- HZI (Helmholtz Centre for Infection Research) (submittedVersion)
- The Journal of the American Medical Association (JAMA) Network (American Medical Association) (submittedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Max Planck Digital Library (submittedVersion)
- DZNE Pub (submittedVersion)
- MPG.PuRe (Max Planck Society) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- National Institutes of Health
- Genentech
- National Heart, Lung, and Blood Institute (R01HL093262)
- National Institute of General Medical Sciences (R01GM054060)
- National Institute of Allergy and Infectious Diseases (U19AI084048, R01AI083713)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- NLRP3 inflammasome, caspase-1, Alzheimer's disease, amyloid-beta, APP/PS1 mice, microglia, neuroinflammation, IL-1β, amyloid-beta clearance, spatial memory, NLRP3 knockout mice, cognitive impairment, therapeutic target
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Aged, Aged, 80 and over, Alzheimer Disease, Animals, Behavior, Animal, Brain, Carrier Proteins, Humans, Memory, Mice, Inbred C57BL, Mice, Transgenic, Phagocytosis, Gene Expression Regulation, Enzymologic, Amyloid beta-Peptides, Caspase 1, Mice, Nitric Oxide Synthase Type II, Interleukin-1beta, Inflammasomes, Cognitive Dysfunction
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
