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
“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 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 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 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
“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
“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
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
Flagged first, then by citations
2 of the 34 references couldn’t be matched to a known paper.
Cited by
Sorted by citations
Items 501–600 of 1,031
Zádori, D., Veres, G., Szalárdy, L., Klivènyi, P., & Vécsei, L. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-170929 · Cited by 108
Zhang, X., He, Q., Huang, T., Zhao, N., Liang, F., Xu, B., Chen, X., Li, T., & Bi, J. (2019) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2019.00078 · Cited by 107
Skelly, D., Griffin, É. W., Murray, C., Harney, S. C., O’Boyle, C., Hennessy, E., Dansereau, M., Nazmi, A., Tortorelli, L. S., Rawlins, J. N. P., et al. (2018) · Molecular Psychiatry · doi:10.1038/s41380-018-0075-8 · Cited by 114
Role of dietary fatty acids in microglial polarization in Alzheimer’s disease
Desale, S. E., & Chinnathambi, S. (2020) · Journal of Neuroinflammation · doi:10.1186/s12974-020-01742-3 · Cited by 112
TRPV1 channel mediates NLRP3 inflammasome-dependent neuroinflammation in microglia
Zhang, Y., Hou, B., Liang, P., Lu, X., Wu, Y., Zhang, X., Fan, Y., Liu, Y., Chen, T.-X., Liu, W., et al. (2021) · Cell Death and Disease · doi:10.1038/s41419-021-04450-9 · Cited by 107
Peng, Y., Gao, P., Shi, L., Chen, L., Liu, J., & Long, J. (2020) · Antioxidants & Redox Signaling · doi:10.1089/ars.2019.7763 · Cited by 110
Rong, S., Wan, D., Fan, Y., Liu, S., Sun, K., Huo, J., Zhang, P., Li, X., Xie, X., Wang, F., et al. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.00856 · Cited by 106
Li, T., Lu, L., Pember, E., Li, X., Zhang, B., & Zhu, Z. (2022) · Cells · doi:10.3390/cells11121925 · Cited by 109
Microglial mitophagy mitigates neuroinflammation in Alzheimer's disease
Lautrup, S., Lou, G., Aman, Y., Nilsen, H., Tao, J., & Fang, E. F. (2019) · Neurochemistry International · doi:10.1016/j.neuint.2019.104469 · Cited by 105
Microglia in Alzheimer’s disease: A target for immunotherapy
Wang, S., & Colonna, M. (2019) · Journal of Leukocyte Biology · doi:10.1002/jlb.mr0818-319r · Cited by 106
Yang, C., Mo, Y., Xu, E., Wen, H., Wei, R., Li, S., Zheng, J., Li, W., Le, L. B., Chen, Y., et al. (2019) · International Immunopharmacology · doi:10.1016/j.intimp.2019.05.036 · Cited by 105
Xiao, L., Zheng, H., Li, J., Wang, Q., & Sun, H. (2020) · Molecular Neurobiology · doi:10.1007/s12035-020-02082-2 · Cited by 107
Miao, J., Chen, L., Pan, X., Li, L.-Q., Zhao, B., & Lan, J. X. (2023) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-023-01376-y · Cited by 121
Liu, L., & Chan, C. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.08.016 · Cited by 108
The role of the immune system in neurodegenerative disorders: Adaptive or maladaptive?
Doty, K. R., Guillot-Sestier, M.-V., & Town, T. (2015) · Brain Research · doi:10.1016/j.brainres.2014.09.008 · Cited by 104
The impact of PKR activation: from neurodegeneration to cancer
Marchal, J. A., López, G., Perán, M., Comino, A., Delgado, J. R., Garcı́a-Garcı́a, J., Conde, V., Aranda, F. M., Rivas, C., Estéban, M., et al. (2014) · The FASEB Journal · doi:10.1096/fj.13-248294 · Cited by 106
Pellegrini, C., Fornai, M., Antonioli, L., Blandizzi, C., & Calderone, V. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20122876 · Cited by 113
Alterations in the Gut-Microbial-Inflammasome-Brain Axis in a Mouse Model of Alzheimer’s Disease
Shukla, P. K., Delotterie, D. F., Xiao, J., Pierre, J. F., Rao, R., McDonald, M. P., & Khan, M. M. (2021) · Cells · doi:10.3390/cells10040779 · Cited by 105
The Multiple Roles of Autophagy in Neural Function and Diseases
Li, Y., Qin, Z., & Sheng, R. (2023) · Neuroscience Bulletin · doi:10.1007/s12264-023-01120-y · Cited by 109
Inflammasomes in neurological disorders — mechanisms and therapeutic potential
Ravichandran, K. A., & Heneka, M. T. (2024) · Nature Reviews Neurology · doi:10.1038/s41582-023-00915-x · Cited by 112
Self-citationNeuroprotective effects of dietary restriction: Evidence and mechanisms
Pani, G. (2015) · Seminars in Cell & Developmental Biology · doi:10.1016/j.semcdb.2015.03.004 · Cited by 103
Chung, S., Jeong, J.-H., Park, J.-C., Han, J. W., Lee, Y., Kim, J.-I., & Mook-Jung, I. (2024) · Experimental & Molecular Medicine · doi:10.1038/s12276-024-01295-y · Cited by 103
“We next investigated the NLRP3 in fl ammasome in microglia because STING has been reported to drive NLRP3 activation in peritoneal macrophages 33, and NLRP3 is critical for AD pathogenesis 34 .”
Innate Immunity Fights Alzheimer's Disease
Guillot‐Sestier, M., Doty, K. R., & Town, T. (2015) · Trends in Neurosciences · doi:10.1016/j.tins.2015.08.008 · Cited by 101
Interactions between inflammation, sex steroids, and Alzheimer’s disease risk factors
Uchoa, M. F., Moser, V. A., & Pike, C. J. (2016) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2016.09.001 · Cited by 105
Zhao, N., Li, C.-C., Di, B., & Xu, L.-L. (2020) · Journal of Autoimmunity · doi:10.1016/j.jaut.2020.102515 · Cited by 103
Pyroptosis, and its Role in Central Nervous System Disease
Hu, Y., Wang, B., Li, S., & Yang, S. (2021) · Journal of Molecular Biology · doi:10.1016/j.jmb.2021.167379 · Cited by 103
Bashir, A., Nabi, M., Tabassum, N., Afzal, S., & Ayoub, M. (2023) · Frontiers in Pharmacology · doi:10.3389/fphar.2023.1049334 · Cited by 121
Mitochondria Dysfunction and Neuroinflammation in Neurodegeneration: Who Comes First?
Peggion, C., Calí, T., & Brini, M. (2024) · Antioxidants · doi:10.3390/antiox13020240 · Cited by 112
Microglia and Astrocytes in Alzheimer’s Disease: Significance and Summary of Recent Advances
Deng, Q., Wu, C., Parker, E., Liu, T. C.-Y., Duan, R., & Yang, L. (2023) · Aging and disease · doi:10.14336/ad.2023.0907 · Cited by 102
Alzheimer’s Disease: Mechanism and Approach to Cell Therapy
Amemori, T., Jendelová, P., Růžička, J., Urdzíková, L. M., & Syková, E. (2015) · International Journal of Molecular Sciences · doi:10.3390/ijms161125961 · Cited by 110
NLRP3 Inflammasome: Activation and Regulation in Age‐Related Macular Degeneration
Gao, J., Liu, R. T., Cao, S., Cui, J. Z., Wang, A., To, E. C., & Matsubara, J. A. (2015) · Mediators of Inflammation · doi:10.1155/2015/690243 · Cited by 105
Zhang, M. Q., Zhao, Q., Xia, M., Chen, J., Chen, Y., Cao, X., Liu, Y., Yuan, Z., Wang, X., & Xu, Y. (2019) · The FASEB Journal · doi:10.1096/fj.201900394rrr · Cited by 101
Lee, A.-H., Shin, H.-Y., Park, J.-H., Koo, S. Y., Kim, S. M., & Yang, S. (2021) · Scientific Reports · doi:10.1038/s41598-020-80748-6 · Cited by 117
Inflammatory caspases: key regulators of inflammation and cell death
Fernández, D. J., & Lamkanfi, M. (2014) · Biological Chemistry · doi:10.1515/hsz-2014-0253 · Cited by 101
Hasegawa, T., Nakashima, M., & Suzuki, Y. (2016) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2016.06.106 · Cited by 101
Du, R., Wu, F.-F., Lu, M., Shu, X.-D., Ding, J.-H., Wu, G., & Hu, G. (2016) · Redox Biology · doi:10.1016/j.redox.2016.08.006 · Cited by 100
Exosomes in Food: Health Benefits and Clinical Relevance in Diseases
Munir, J., Lee, M., & Ryu, S. (2019) · Advances in Nutrition · doi:10.1093/advances/nmz123 · Cited by 100
Exploring the Multifaceted Therapeutic Potential of Withaferin A and Its Derivatives
Behl, T., Sharma, A., Sharma, L. K., Sehgal, A., Zengin, G., Brata, R. D., Frățilă, O., & BUNGAU, S. G. (2020) · Biomedicines · doi:10.3390/biomedicines8120571 · Cited by 100
Microglia dynamics in aging-related neurobehavioral and neuroinflammatory diseases
Javanmehr, N., Saleki, K., Alijanizadeh, P., & Rezaei, N. (2022) · Journal of Neuroinflammation · doi:10.1186/s12974-022-02637-1 · Cited by 106
Ganguli, M. (2015) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0000000000000086 · Cited by 100
Wang, J., Ren, H., Yuan, X., Ma, H., Shi, X., & Ding, Y. (2017) · Hepatology Research · doi:10.1111/hepr.12969 · Cited by 99
Neuronal SphK1 acetylates COX2 and contributes to pathogenesis in a model of Alzheimer’s Disease
Lee, J. Y., Han, S. H., Park, M. H., Baek, B., Song, I., Choi, M.-K., Takuwa, Y., Ryu, H., Kim, S. H., He, X., et al. (2018) · Nature Communications · doi:10.1038/s41467-018-03674-2 · Cited by 98
Alzheimer’s Disease and Inflammaging
Kosyreva, A., Sentyabreva, A., Tsvetkov, I., & Makarova, O. (2022) · Brain Sciences · doi:10.3390/brainsci12091237 · Cited by 98
Microglia responses to interleukin‐6 and type I interferons in neuroinflammatory disease
West, P. K., Viengkhou, B., Campbell, I. L., & Hofer, M. J. (2019) · Glia · doi:10.1002/glia.23634 · Cited by 101
Medrano-Jiménez, E., Jiménez-Ferrer, I., Pedraza‐Escalona, M., Ramírez-Serrano, C. E., Álvarez‐Arellano, L., Cortés‐Mendoza, J., Herrera-Ruiz, M. L., Jiménez‐Ferrer, E., Zamilpa, A., Tortoriello, J., et al. (2019) · Journal of Neuroinflammation · doi:10.1186/s12974-019-1515-3 · Cited by 100
Flores, J., Noël, A., Foveau, B., Beauchet, O., & LeBlanc, A. C. (2020) · Nature Communications · doi:10.1038/s41467-020-18405-9 · Cited by 103
Microglia and astrocyte involvement in neurodegeneration and brain cancer
Vandenbark, A. A., Offner, H., Matejuk, S., & Matejuk, A. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02355-0 · Cited by 101
Long, H., Zhou, Z.-W., Cheng, Y., Luo, H., Li, F., Xu, S., & Gao, L. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.888989 · Cited by 100
Xu, L., Gao, H., Zhan, W., Deng, Y., Liu, X., Jiang, Q., Sun, X., Xu, J., & Liang, G. (2023) · Journal of the American Chemical Society · doi:10.1021/jacs.3c10255 · Cited by 98
Neuroinflammation, immune system and Alzheimer disease: searching for the missing link
Guerriero, F., Sgarlata, C. S., Francis, M., Maurizi, N., Faragli, A., Perna, S., Rondanelli, M., Rollone, M., & Ricevuti, G. (2016) · Aging Clinical and Experimental Research · doi:10.1007/s40520-016-0637-z · Cited by 98
PINK1/Parkin-Dependent Mitochondrial Surveillance: From Pleiotropy to Parkinson's Disease
Mouton‐Liger, F., Jacoupy, M., Corvol, J., & Corti, O. (2017) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2017.00120 · Cited by 100
Chronic murine toxoplasmosis is defined by subtle changes in the neuronal connectivity
Parlog, A., Harsan, L. A., Zagrebelsky, M., Weller, M., von Elverfeldt, D., Mawrin, C., Körte, M., & Dunay, I. R. (2014) · Disease Models & Mechanisms · doi:10.1242/dmm.014183 · Cited by 99
Hydroxytyrosol mildly improve cognitive function independent of APP processing in APP/PS1 mice
Peng, Y., Hou, C., Yang, Z., Li, C., Jia, L., Liu, J., Tang, Y., Shi, L., Li, Y., Long, J., et al. (2016) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.201600332 · Cited by 103
Naeem, A., Prakash, R., Kumari, N., Ali Khan, M., Quaiyoom Khan, A., Uddin, S., Verma, S., AB Robertson, A., Boltze, J., & Shadab Raza, S. (2024) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2023.11.031 · Cited by 96
Keaney, J., Gasser, J., Gillet, G., Scholz, D., & Kadiu, I. (2019) · Journal of Neuroimmune Pharmacology · doi:10.1007/s11481-019-09839-0 · Cited by 98
Gabandé‐Rodríguez, E., Heras, M. M. G. D. L., & Mittelbrunn, M. (2019) · Cells · doi:10.3390/cells9010082 · Cited by 101
Li, D., Tian, H., Li, X., Mao, L., Zhao, X., Lin, J., Lin, S., Xu, C., Liu, Y., Guo, Y., et al. (2020) · Life Sciences · doi:10.1016/j.lfs.2020.117351 · Cited by 96
ER stress activates immunosuppressive network: implications for aging and Alzheimer’s disease
Salminen, A., Kaarniranta, K., & Kauppinen, A. (2020) · Journal of Molecular Medicine · doi:10.1007/s00109-020-01904-z · Cited by 99
Resting State fMRI and Improved Deep Learning Algorithm for Earlier Detection of Alzheimer’s Disease
Guo, H., & Zhang, Y. (2020) · IEEE Access · doi:10.1109/access.2020.3003424 · Cited by 99
Couturier, J., Stancu, I., Schakman, O., Pierrot, N., Huaux, F., Kienlen‐Campard, P., Dewachter, I., & Octave, J. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0477-y · Cited by 95
Terzioglu, G., & Young-Pearse, T. L. (2023) · Molecular Neurodegeneration · doi:10.1186/s13024-023-00674-9 · Cited by 91
Diverse activation of microglia by chemokine (C-C motif) ligand 2 overexpression in brain
Selenica, M. B., Alvarez, J. A., Nash, K. R., Lee, D. C., Cao, C., Lin, X., Reid, P., Mouton, P. R., Morgan, D., & Gordon, M. N. (2013) · Journal of Neuroinflammation · doi:10.1186/1742-2094-10-86 · Cited by 99
Cerebrovascular complications of diabetes: focus on cognitive dysfunction
Hardigan, T., Ward, R., & Ergul, A. (2016) · Clinical Science · doi:10.1042/cs20160397 · Cited by 100
Burchfield, J. G., Kebede, M. A., Meoli, C. C., Stöckli, J., Whitworth, P. T., Wright, A. L., Hoffman, N. J., Minard, A. Y., Ma, X., Krycer, J. R., et al. (2018) · Journal of Biological Chemistry · doi:10.1074/jbc.ra117.000808 · Cited by 97
Role of pyroptosis in the pathogenesis of various neurological diseases
Oladapo, A., Jackson, T., Menolascino, J., & Periyasamy, P. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.02.001 · Cited by 101
Scala, F., Fusco, S., Ripoli, C., Piacentini, R., Puma, D. D. L., Spinelli, M., Laezza, F., Grassi, C., & D’Ascenzo, M. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.10.034 · Cited by 98
Longitudinal follow-up of autophagy and inflammation in brain of APPswePS1dE9 transgenic mice
François, A., Bilan, A. R., Quellard, N., Fernandez, B., Janet, T., Chassaing, D., Paccalin, M., Terro, F., & Page, G. (2014) · Journal of Neuroinflammation · doi:10.1186/s12974-014-0139-x · Cited by 98
Type-I interferon pathway in neuroinflammation and neurodegeneration: focus on Alzheimer’s disease
Taylor, J. M., Moore, Z., Minter, M. R., & Crack, P. J. (2017) · Journal of Neural Transmission · doi:10.1007/s00702-017-1745-4 · Cited by 94
Is Alzheimer’s disease an inflammasomopathy?
Pereira, C., Santos, A. E., Moreira, P. I., Pereira, A. C., Sousa, F. J., Cardoso, S. M., & Cruz, M. T. (2019) · Ageing Research Reviews · doi:10.1016/j.arr.2019.100966 · Cited by 95
Rexach, J. E., Polioudakis, D., Yin, A., Swarup, V., Chang, T. S., Nguyen, T., Sarkar, A., Chen, L., Huang, J., Lin, L.-C., et al. (2020) · Cell Reports · doi:10.1016/j.celrep.2020.108398 · Cited by 94
Bibliometric Analysis of the Inflammasome and Pyroptosis in Brain
Chen, Y., Li, Y., Guo, L., Hong, J. Y., Zhao, W., Hu, X., Chang, C., Liu, W., & Xiong, K. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2020.626502 · Cited by 94
Redox regulation of macrophages
Tran, N., & Mills, E. L. (2024) · Redox Biology · doi:10.1016/j.redox.2024.103123 · Cited by 101
Proteostasis and lysosomal repair deficits in transdifferentiated neurons of Alzheimer’s disease
Chou, C.-C., Vest, R., Prado, M. A., Wilson-Grady, J., Paulo, J. A., Shibuya, Y., Moran-Losada, P., Lee, T.-T., Luo, J., Gygi, S. P., et al. (2025) · Nature Cell Biology · doi:10.1038/s41556-025-01623-y · Cited by 94
An, Y. W., Jhang, K. A., Woo, S., Kang, J. L., & Chong, Y. H. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.10.016 · Cited by 95
Inflammasome-mediated innate immunity in Alzheimer’s disease
Venegas, C., & Heneka, M. T. (2019) · The FASEB Journal · doi:10.1096/fj.201900439 · Cited by 93
Self-citationThe NLRP3 inflammasome: Role in metabolic disorders and regulation by metabolic pathways
Jiang, D., Chen, S., Sun, R., Zhang, X., & Wang, D. (2018) · Cancer Letters · doi:10.1016/j.canlet.2018.01.034 · Cited by 95
The Gut-Brain Axis in Alzheimer’s Disease and Omega-3. A Critical Overview of Clinical Trials
Rosa, F. L., Clerici, M., Ratto, D., Occhinegro, A., Licito, A., Romeo, M., Iorio, C. D., & Rossi, P. (2018) · Nutrients · doi:10.3390/nu10091267 · Cited by 96
Specific Inhibition of the NLRP3 Inflammasome as an Antiinflammatory Strategy in Cystic Fibrosis
McElvaney, O. J., Zasłona, Z., Becker-Flegler, K. A., Pålsson‐McDermott, E. M., Boland, F., Gunaratnam, C., Gulbins, E., O'Neill, L. A. J., Reeves, E. P., & McElvaney, N. G. (2019) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.201905-1013oc · Cited by 97
Immunotherapies for Aging-Related Neurodegenerative Diseases—Emerging Perspectives and New Targets
Kwon, S., Iba, M., Kim, C., & Masliah, E. (2020) · Neurotherapeutics · doi:10.1007/s13311-020-00853-2 · Cited by 97
Fueling neurodegeneration: metabolic insights into microglia functions
Sadeghdoust, M., Das, A., & Kaushik, D. K. (2024) · Journal of Neuroinflammation · doi:10.1186/s12974-024-03296-0 · Cited by 107
Resveratrol and Alzheimer’s disease: message in a bottle on red wine and cognition
Granzotto, A., & Zatta, P. F. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00095 · Cited by 99
Jiang, S., Maphis, N. M., Binder, J., Chisholm, D., Weston, L., Duran, W., Peterson, C., Zimmerman, A., Mandell, M. A., Jett, S. D., et al. (2021) · Cell Reports · doi:10.1016/j.celrep.2021.109720 · Cited by 92
Self-citationFeng, S.-T., Wang, Z.-Z., Yuan, Y.-H., Sun, H.-M., Chen, N.-H., & Zhang, Y. (2019) · Pharmacological Research · doi:10.1016/j.phrs.2019.104336 · Cited by 96
Myeloperoxidase and Neurological Disorder: A Crosstalk
Pravalika, K., Sarmah, D., Kaur, H., Wanve, M., Saraf, J., Kalia, K., Borah, A., Yavagal, D. R., Dave, K. R., & Bhattacharya, P. (2018) · ACS Chemical Neuroscience · doi:10.1021/acschemneuro.7b00462 · Cited by 91
Antimicrobial Peptide LL-37 Drives Rosacea-Like Skin Inflammation in an NLRP3-Dependent Manner
Yoon, S.-H., Hwang, I., Lee, E., Cho, H.-J., Ryu, J. H., Kim, T., & Yu, J. (2021) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2021.02.745 · Cited by 94
Zalpoor, H., Akbari, A., Samei, A., Forghaniesfidvajani, R., Kamali, M., Afzalnia, A., Manshouri, S., Heidari, F., Pornour, M., Khoshmirsafa, M., et al. (2022) · Cellular & Molecular Biology Letters · doi:10.1186/s11658-022-00311-1 · Cited by 92
Gullotta, G. S., Costantino, G., Sortino, M. A., & Spampinato, S. F. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24119144 · Cited by 97
Iron Toxicity in the Retina Requires Alu RNA and the NLRP3 Inflammasome
Gelfand, B. D., Wright, C. B., Kim, Y., Yasuma, T. R., Yasuma, R., Li, S., Fowler, B. J., Bastos-Carvalho, A., Kerur, N., Uittenbogaard, A., et al. (2015) · Cell Reports · doi:10.1016/j.celrep.2015.05.023 · Cited by 92
Liu, Y. F., Jing, Y.-Y., Zeng, C., Li, C., Xu, L., Liang, Y., Bai, W.-J., Zha, Q., Ouyang, D., & He, X. (2018) · Frontiers in Pharmacology · doi:10.3389/fphar.2017.00975 · Cited by 91
Wiciński, M., Socha, M. W., Malinowski, B., Wódkiewicz, E., Walczak, M., Górski, K. M., Słupski, M., & Pawlak-Osińska, K. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20051050 · Cited by 94
Hughes, M. M., Hooftman, A., Angiari, S., Tummala, P., Zasłona, Z., Runtsch, M. C., McGettrick, A. F., Sutton, C. E., Diskin, C., Rooke, M., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.08.072 · Cited by 94
The role of NLRP3 inflammasome in aging and age-related diseases
Liang, R., Qi, X., Cai, Q., Niu, L., Huang, X., Zhang, D., Ling, J., Wu, Y., Chen, Y., Yang, P., et al. (2024) · Immunity & Ageing · doi:10.1186/s12979-023-00395-z · Cited by 98
Boini, K. M., Xia, M., Abais, J. M., Li, G., Pitzer, A. L., Gehr, T. W. B., Zhang, Y., & Li, P. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Cell Research · doi:10.1016/j.bbamcr.2014.01.033 · Cited by 91
Resveratrol inhibits the acetylated α-tubulin-mediated assembly of the NLRP3-inflammasome
Misawa, T., Saitoh, T., Kozaki, T., Park, S., Takahama, M., & Akira, S. (2015) · International Immunology · doi:10.1093/intimm/dxv018 · Cited by 93
Feng, L., & Zhang, L. (2019) · DNA and Cell Biology · doi:10.1089/dna.2018.4308 · Cited by 90
Obesity and sex interact in the regulation of Alzheimer's disease
Moser, V. A., & Pike, C. J. (2015) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2015.08.021 · Cited by 91
viringipurampeer, I. A., Metcalfe, A. L., Bashar, E., Sivak, O., Yanai, A., Mohammadi, Z., Moritz, O. L., Gregory, C. Y., & Gregory-Evans, K. (2016) · Human Molecular Genetics · doi:10.1093/hmg/ddw029 · Cited by 90
Reifschneider, A., Robinson, S., van Lengerich, B., Gnörich, J., Logan, T., Heindl, S., Vogt, M. A., Weidinger, E., Riedl, L., Wind, K., et al. (2022) · The EMBO Journal · doi:10.15252/embj.2021109108 · Cited by 89
Activation of the NLRP3 inflammasome by cellular labile iron
Nakamura, K., Kawakami, T., Yamamoto, N., Tomizawa, M., Fujiwara, T., Ishii, T., Harigae, H., & Ogasawara, K. (2015) · Experimental Hematology · doi:10.1016/j.exphem.2015.11.002 · Cited by 89
Quarta, C., Clemmensen, C., Zhu, Z., Yang, B. S., Joseph, S. S., Lutter, D., Yi, C., Graf, E., García‐Cáceres, C., Legutko, B., et al. (2017) · Cell Metabolism · doi:10.1016/j.cmet.2017.08.023 · Cited by 89
Self-citation
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
