Ablation of TNF-RI/RII Expression in Alzheimer's Disease Mice Leads to an Unexpected Enhancement of Pathology
Open accessAbstract
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by severe memory loss and cognitive impairment. Neuroinflammation, including the extensive production of pro-inflammatory molecules and the activation of microglia, has been implicated in the disease process. Tumor necrosis factor (TNF)-α, a prototypic pro-inflammatory cytokine, is elevated in AD, is neurotoxic, and colocalizes with amyloid plaques in AD animal models and human brains. We previously demonstrated that the expression of TNF-α is increased in AD mice at ages preceding the development of hallmark amyloid and tau pathological features and that long-term expression of this cytokine in these mice leads to marked neuronal death. Such observations suggest that TNF-α signaling promotes AD pathogenesis and that therapeutics suppressing this cytokine's activity may be beneficial. To dissect TNF-α receptor signaling requirements in AD, we generated triple-transgenic AD mice (3xTg-AD) lacking both TNF-α receptor 1 (TNF-RI) and 2 (TNF-RII), 3xTg-ADxTNF-RI/RII knock out, the cognate receptors of TNF-α. These mice exhibit enhanced amyloid and tau-related pathological features by the age of 15 months, in stark contrast to age-matched 3xTg-AD counterparts. Moreover, 3xTg-ADxTNF-RI/RII knock out-derived primary microglia reveal reduced amyloid-β phagocytic marker expression and phagocytosis activity, indicating that intact TNF-α receptor signaling is critical for microglial-mediated uptake of extracellular amyloid-β peptide pools. Overall, our results demonstrate that globally ablated TNF receptor signaling exacerbates pathogenesis and argues against long-term use of pan-anti-TNF-α inhibitors for the treatment of AD.
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Microglia from TNFR-deficient 3xTgAD mice show defective phagocytosis, highlighting a protective role for TNF-α in clearance mechanisms.
“microglia from TNFR-deficient 3xTgAD mice showed defective phagocytosis, highlighting the protective role of TNF-α in facilitating clearance mechanisms.”
From Microglia in Alzheimer's disease (2017) · cites this paper as [129]
TNFR deficiency in 3xTgAD mice is associated with increased amyloid deposition and enhanced tau phosphorylation.
“TNF receptor (TNFR) deficiency in 3xTgAD mice was associated with increased amyloid deposition and enhanced tau phosphorylation (129).”
From Microglia in Alzheimer's disease (2017) · cites this paper as [129]
Global knockout of TNFR1 and TNFR2 receptors in 3xTg mice worsened Aβ and tau pathology.
“another group found that global knockout of TNFR1 and TNFR2 receptors in 3xTg mice worsened Aβ and tau pathology [149].”
From Glial contributions to neurodegeneration in tauopathies (2017) · cites this paper as [149]
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- Authors
- Montgomery, S. L., Mastrangelo, M. A., Habib, D., Narrow, W. C., Knowlden, S. A., Wright, T. W., & Bowers, W. J.
- Affiliations
- University of Rochester Medicine (US)
- Corresponding author
- Bowers, William J.
- Venue
- The American Journal of Pathology
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 179
- Issue
- 4
- Pages
- 2053-2070
- ISSN
- 0002-9440 (ISSN-L)
- PMC
- PMC3181376
- OpenAlex
- W10297594
- Cited by
- 96
- References
- 112
- Citations by year
- 2024: 2 · 2023: 7 · 2022: 4 · 2021: 13 · 2020: 9 · 2019: 6 · 2018: 6 · 2017: 10 · 2016: 6 · 2015: 9 · 2014: 11 · 2013: 8 · 2012: 5
- FWCI
- 5.23
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- American Journal Of Pathology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (F31-AG038063, R01-AG023593, R01-AG026328)
- 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, TNF receptor 1, TNF receptor 2, TNF signaling, neuroinflammation, microglia, amyloid-beta phagocytosis, amyloid plaques, tau pathology, 3xTg-AD mice, anti-TNF therapy, receptor knockout mice
- MeSH terms
- Aging, Alzheimer Disease, Amyloid, Animals, Brain, Calcium-Binding Proteins, Crosses, Genetic, Female, Humans, Male, Microfilament Proteins, Phagocytosis, Synapses, Tumor Necrosis Factor-alpha, Amyloid beta-Protein Precursor, tau Proteins, Microglia, Long-Term Potentiation, Mice, Knockout, Lipopolysaccharide Receptors, Transgenes, Receptors, Tumor Necrosis Factor, Type I, Receptors, Tumor Necrosis Factor, Type II, Adaptor Proteins, Signal Transducing, Mice, CA1 Region, Hippocampal, CA3 Region, Hippocampal
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.
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