Blocking IL-1 Signaling Rescues Cognition, Attenuates Tau Pathology, and Restores Neuronal β-Catenin Pathway Function in an Alzheimer’s Disease Model
Open accessAbstract
Inflammation is a key pathological hallmark of Alzheimer’s disease (AD), although its impact on disease progression and neurodegeneration remains an area of active investigation. Among numerous inflammatory cytokines associated with AD, IL-1β in particular has been implicated in playing a pathogenic role. In this study, we sought to investigate whether inhibition of IL-1β signaling provides disease-modifying benefits in an AD mouse model and, if so, by what molecular mechanisms. We report that chronic dosing of 3xTg-AD mice with an IL-1R blocking Ab significantly alters brain inflammatory responses, alleviates cognitive deficits, markedly attenuates tau pathology, and partly reduces certain fibrillar and oligomeric forms of amyloid-β. Alterations in inflammatory responses correspond to reduced NF-κB activity. Furthermore, inhibition of IL-1 signaling reduces the activity of several tau kinases in the brain, including cdk5/p25, GSK-3β, and p38–MAPK, and also reduces phosphorylated tau levels. We also detected a reduction in the astrocyte-derived cytokine, S100B, and in the extent of neuronal Wnt/β-catenin signaling in 3xTg-AD brains, and provided in vitro evidence that these changes may, in part, provide a mechanistic link between IL-1 signaling and GSK-3β activation. Taken together, our results suggest that the IL-1 signaling cascade may be involved in one of the key disease mechanisms for AD.
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Pathological activation of glial cells and release of inflammatory factors involved in neuroinflammation can exacerbate tau pathology via direct or indirect pathways, leading to neuronal damage and cognitive impairment, ultimately aggravating AD pathology.
“Evidence suggests that the pathological activation of glial cells and the release of inflammatory factors involved in neuroinflammation can exacerbate tau pathology via direct or indirect pathways, leading to neuronal damage and cognitive impairment, ultimately aggravating AD pathology [113, 114].”
From Tau and neuroinflammation in Alzheimer’s disease: interplay mechanisms and clinical translation (2023) · cites this paper as [113]
Proinflammatory cytokines TNFα, IL1β, and IL6 promote tau phosphorylation in neurons.
“First, the proinflammatory cytokines TNFα, IL1 β, and IL6 have been shown to promote tau phosphorylation in neurons (Bhaskar et al., 2010; Kitazawa et al., 2011; Quintanilla et al., 2004).”
From Complement C3aR Inactivation Attenuates Tau Pathology and Reverses an Immune Network Deregulated in Tauopathy Models and Alzheimer’s Disease (2018) · cites this paper as Kitazawa et al., 2011
IL-1 receptor signalling plays a key role in neuroinflammation-induced tau phosphorylation by enhancing the activity of tau kinases including CDK5/p25, GSK3β, and p38-MAPK.
“IL-1 receptor signalling is found to play a key role in neuroinflammation-induced tau phosphorylation by enhancing the activity of tau kinases including cyclin-dependent-like kinase 5/p25 (CDK5/p25), glycogen synthase kinase 3β (GSK3β), and p38 mitogen-activated protein kinase (p38-MAPK)60,61.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [61]
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- Authors
- Kitazawa, M., Cheng, D., Tsukamoto, M. R., Koike, M. A., Wes, P. D., Vasilevko, V., Cribbs, D. H., & LaFerla, F. M.
- Affiliations
- University of California, Irvine (US)
- Roche Pharmaceuticals , Palo Alto, CA 94304
- Corresponding author
- Kitazawa, Masashi
- Cheng, David
- Vasilevko, Vitaly
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-12
- Volume
- 187
- Issue
- 12
- Pages
- 6539-6549
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- PMC
- PMC4072218
- OpenAlex
- W2129470375
- Cited by
- 473
- References
- 83
- Citations by year
- 2026: 32 · 2025: 42 · 2024: 40 · 2023: 36 · 2022: 43 · 2021: 35 · 2020: 46 · 2019: 31 · 2018: 39 · 2017: 26 · 2016: 30 · 2015: 18 · 2014: 24 · 2013: 17 · 2012: 14
- FWCI
- 11.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (4r01ag020241-15)
- National Institute on Aging (P01AG000538, R01AG020335, P50 AG 16573, R01 AG-020241, AG020241, AG 00538, P50AG016573, RF1AG020241, R01AG20335, R01AG021982)
- National Institute of Neurological Disorders and Stroke (NS 050895, R01NS050895)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (K99AR054695)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, IL-1β signaling, IL-1 receptor blockade, tau pathology, cognitive impairment, amyloid-beta, NF-κB, tau kinases, GSK3β, CDK5/p25, p38 MAPK, Wnt/β-catenin signaling, S100B, astrocytes, neuroinflammation, 3xTg-AD mice, disease-modifying therapy
- MeSH terms
- Alzheimer Disease, Animals, Cells, Cultured, Cognition Disorders, Disease Models, Animal, Female, Humans, Male, Mice, Inbred C57BL, Mice, Transgenic, Nerve Growth Factors, S100 Proteins, Neurons, Signal Transduction, NF-kappa B, tau Proteins, Receptors, Interleukin-1, Cell Line, Tumor, beta Catenin, Mice, Interleukin-1beta, S100 Calcium Binding Protein beta Subunit
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