Cited by 473Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

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Blocking IL-1 Signaling Rescues Cognition, Attenuates Tau Pathology, and Restores Neuronal β-Catenin Pathway Function in an Alzheimer’s Disease Model

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Kitazawa, Masashi, Cheng, David, Tsukamoto, Michelle R, Koike, Maya A, Wes, Paul D, Vasilevko, Vitaly, Cribbs, David H, LaFerla, Frank M·2011·The Journal of Immunology

DOI 10.4049/jimmunol.1100620PMC PMC4072218

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Abstract

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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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
ORCID: Kitazawa, Masashi
Cheng, David
Wes, Paul D
Cribbs, David H
LaFerla, Frank M
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
DOI: 10.4049/jimmunol.1100620
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
Licence: academic.oup.com/pages/standard-publication-reuse-rights (vor)
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: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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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Blocking IL-1 Signaling Rescues Cognition, Attenuates Tau Pathology, and Restores Neuronal β-Catenin Pathway Function in an Alzheimer’s Disease Model

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