Cited by 367Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsNeuroscience and Neuropharmacology Research

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Interferon-γ and Tumor Necrosis Factor-α Regulate Amyloid-β Plaque Deposition and β-Secretase Expression in Swedish Mutant APP Transgenic Mice

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Yamamoto, Masaru, Kiyota, Tomomi, Horiba, Masahide, Buescher, James L., Walsh, Shannon M., Gendelman, Howard E., Ikezu, Tsuneya·2007·The American Journal of Pathology

DOI 10.2353/ajpath.2007.060378PMC PMC1851864

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Abstract

Reactive astrocytes and microglia in Alzheimer's disease surround amyloid plaques and secrete proinflammatory cytokines that affect neuronal function. Relationship between cytokine signaling and amyloid-beta peptide (Abeta) accumulation is poorly understood. Thus, we generated a novel Swedish beta-amyloid precursor protein mutant (APP) transgenic mouse in which the interferon (IFN)-gamma receptor type I was knocked out (APP/GRKO). IFN-gamma signaling loss in the APP/GRKO mice reduced gliosis and amyloid plaques at 14 months of age. Aggregated Abeta induced IFN-gamma production from co-culture of astrocytes and microglia, and IFN-gamma elicited tumor necrosis factor (TNF)-alpha secretion in wild type (WT) but not GRKO microglia co-cultured with astrocytes. Both IFN-gamma and TNF-alpha enhanced Abeta production from APP-expressing astrocytes and cortical neurons. TNF-alpha directly stimulated beta-site APP-cleaving enzyme (BACE1) expression and enhanced beta-processing of APP in astrocytes. The numbers of reactive astrocytes expressing BACE1 were increased in APP compared with APP/GRKO mice in both cortex and hippocampus. IFN-gamma and TNF-alpha activation of WT microglia suppressed Abeta degradation, whereas GRKO microglia had no changes. These results support the idea that glial IFN-gamma and TNF-alpha enhance Abeta deposition through BACE1 expression and suppression of Abeta clearance. Taken together, these observations suggest that proinflammatory cytokines are directly linked to Alzheimer's disease pathogenesis.

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Authors: Yamamoto, M., Kiyota, T., Horiba, M., Buescher, J. L., Walsh, S. M., Gendelman, H. E., & Ikezu, T.
Affiliations: Nebraska Medical Center (US)
University of Nebraska Medical Center (US)
Corresponding author: Ikezu, Tsuneya
ORCID: Kiyota, Tomomi
Walsh, Shannon M.
Gendelman, Howard E.
Ikezu, Tsuneya
Venue: The American Journal of Pathology
Publisher: Elsevier BV
Published: 2007-02
Volume: 170
Issue: 2
Pages: 680-692
ISSN: 0002-9440 (ISSN-L)
DOI: 10.2353/ajpath.2007.060378
PMC: PMC1851864
OpenAlex: W2062084653
Cited by: 367
References: 62
Citations by year: 2026: 6 · 2025: 14 · 2024: 16 · 2023: 16 · 2022: 19 · 2021: 26 · 2020: 21 · 2019: 19 · 2018: 23 · 2017: 18 · 2016: 18 · 2015: 16 · 2014: 25 · 2013: 22 · 2012: 20
FWCI: 14.54
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: American Journal Of Pathology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: Fondation pour la Recherche sur Alzheimer
National Institutes of Health
National Institute of Neurological Disorders and Stroke (P01NS043985)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Keywords: Alzheimer's disease, amyloid plaques, interferon-gamma, TNF-α, beta-secretase, BACE1, APP transgenic mice, astrocytes, microglia, gliosis, inflammatory cytokines, amyloid-beta clearance, amyloid beta degradation, APP processing
MeSH terms: Interferon gamma Receptor, Alzheimer Disease, Animals, Astrocytes, Cells, Cultured, Cerebellar Cortex, Enzyme Activation, Gliosis, Humans, Interferon-gamma, Neurons, Tumor Necrosis Factor-alpha, Signal Transduction, Gene Expression Regulation, Enzymologic, Amyloid beta-Peptides, Aspartic Acid Endopeptidases, Receptors, Interferon, Microglia, Mice, Knockout, Coculture Techniques, Mice, Amyloid Precursor Protein Secretases, Plaque, Amyloid

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Interferon-γ and Tumor Necrosis Factor-α Regulate Amyloid-β Plaque Deposition and β-Secretase Expression in Swedish Mutant APP Transgenic Mice

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