Deficiency of terminal complement pathway inhibitor promotes neuronal tau pathology and degeneration in mice
Open accessAbstract
BACKGROUND: The neuronal microtubule-associated protein tau becomes hyperphosphorylated and forms aggregates in tauopathies but the processes leading to this pathological hallmark are not understood. Because tauopathies are accompanied by neuroinflammation and the complement cascade forms a key innate immune pathway, we asked whether the complement system has a role in the development of tau pathology. FINDINGS: We tested this hypothesis in two mouse models, which expressed either a central inhibitor of complement or lacked an inhibitor of the terminal complement pathway. Complement receptor-related gene/protein y is the natural inhibitor of the central complement component C3 in rodents. Expressing a soluble variant (sCrry) reduced the number of phospho-tau (AT8 epitope) positive neurons in the brain stem, cerebellum, cortex, and hippocampus of aged P301L mutant tau/sCrry double-transgenic mice compared with tau single-transgenic littermates (JNPL3 line). CD59a is the major inhibitor of formation of the membrane attack complex in mice. Intrahippocampal injection of adeno-associated virus encoding mutant human P301L tau into Cd59a-/- mice resulted in increased numbers of AT8-positive cells compared with wild-type controls. This was accompanied by neuronal and synaptic loss and reduced dendritic integrity. CONCLUSIONS: Our data in two independent mouse models with genetic changes in key regulators of the complement system support the hypothesis that the terminal pathway has an active role in the development of tau pathology. We propose that inhibition of the terminal pathway may be beneficial in tauopathies.
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Multiple studies have shown that complement factor inhibition ameliorates synapse and neuron loss.
“Additionally, multiple studies have shown that complement factor inhibition ameliorates synapse and neuron loss [90–93].”
From Age, sex and Alzheimer’s disease: a longitudinal study of 3xTg-AD mice reveals sex-specific disease trajectories and inflammatory responses mirrored in postmortem brains from Alzheimer’s patients (2024) · cites this paper as [91]
The Findings (page unavailable) report that mice lacking the complement inhibitor CD59a had greater neuronal and synaptic degeneration, while expression of another complement inhibitor reduced phosphorylated-tau-positive neurons. The paper proposes that terminal-pathway inhibition may be beneficial, but it does not show that inhibition ameliorated synapse and neuron loss or report multiple studies demonstrating that outcome. (LLM, conf=0.86)
Experimental — accuracy not yet measuredC3 inhibition by transgenic expression of a soluble form of the mouse complement inhibitory protein Crry reduced the extent of tau pathology.
“C3 inhibition by transgenic expression of a soluble form of the mouse complement inhibitory protein Crry (Britschgi et al., 2012) or C5aR antagonism (Fonseca et al., 2009) reduced the extent of tau pathology.”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Britschgi et al., 2012
Knockout of CD59 worsened pathology in a tau mouse model.
“Knockout of CD59, a protein that inhibits C5b-9 membrane attack complex formation, worsened pathology in a tau mouse model (Britschgi et al., 2012).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Britschgi et al., 2012
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- Authors
- Britschgi, M., Takeda-Uchimura, Y., Rockenstein, E., Johns, H., Masliah, E., & Wyss-Coray, T.
- Affiliations
- Stanford Medicine (US)
- University of California San Diego (US)
- Corresponding author
- Britschgi, Markus
- Venue
- Journal of Neuroinflammation
- Published
- 2012-09-18
- Volume
- 9
- Issue
- 1
- Pages
- 220-220
- ISSN
- 1742-2094 (ISSN-L)
- PMC
- PMC3511294
- OpenAlex
- W2119948079
- Cited by
- 45
- References
- 26
- Citations by year
- 2025: 2 · 2024: 9 · 2023: 4 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 2 · 2018: 2 · 2017: 2 · 2016: 5 · 2015: 2 · 2014: 3 · 2013: 7
- FWCI
- 2.57
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Neuroinflammation (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Science Foundation
- U.S. Department of Veterans Affairs
- University of South Carolina
- Cardiff University
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (102096)
- National Institutes of Health (AG‐18440, AG10435)
- National Institute on Aging (P01AG010435, R37AG018440, AG20603, R01AG027505, R01AG020603, AG 18440, AG02074, AG27505, AG10435)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Immunology and Microbiology › Immunology › Complement system in diseases
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- tauopathy, tau hyperphosphorylation, terminal complement pathway, complement inhibition, Crry, membrane attack complex, neuroinflammation, neurodegeneration, P301L tau, synaptic loss, innate immunity
- MeSH terms
- Animals, Brain, Disease Models, Animal, Humans, Leucine, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Nerve Tissue Proteins, Neurons, Phosphorylation, Proline, Receptors, Complement, Signal Transduction, tau Proteins, CD59 Antigens, Neurodegenerative Diseases, Tauopathies, Green Fluorescent Proteins, Mice
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 ›
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