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NLRP3 inflammasome activation drives tau pathology
Christina Ising, Carmen Venegas, Shuangshuang Zhang, Hannah Scheiblich, Susanne V. Schmidt, Ana Maria Menezes Vieira-Saecker, Stephanie Schwartz, Shadi Albasset, Róisín M. McManus, Darío Tejera, Angelika Griep, Francesco Santarelli, Frederic Brosseron, Sabine Opitz, James Stunden, Maximilian Merten, Rakez Kayed, Douglas Taylor Golenbock, David L Blum, Eicke Latz, Luc Buée, Michael Thomas Heneka. Nature, 2019-11-20
Topic: Brain proteins, microglia and lab models
This study investigated the effect of NLRP3 inflammasome function on tau pathology and Alzheimer's disease progression. The researchers found that loss of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation by regulating tau kinases and phosphatases. Additionally, tau activated the NLRP3 inflammasome, and intracerebral injection of fibrillar amyloid-beta-containing brain homogenates induced tau pathology in an NLRP3-dependent manner.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Ising, C., Venegas, C., Zhang, S., Scheiblich, H., Schmidt, S. V., Vieira-Saecker, A. M. M., et al. (2019). NLRP3 inflammasome activation drives tau pathology. Nature. https://doi.org/10.1038/s41586-019-1769-z
Vancouver
Ising C, Venegas C, Zhang S, Scheiblich H, Schmidt SV, Vieira-Saecker AMM, et al. NLRP3 inflammasome activation drives tau pathology. Nature. 2019. doi:10.1038/s41586-019-1769-z. PMID: 31748742.
BibTeX
@article{ising2019-31748742,
author = {Ising, Christina and Venegas, Carmen and Zhang, Shuangshuang and Scheiblich, Hannah and Schmidt, Susanne V. and Vieira-Saecker, Ana Maria Menezes and Schwartz, Stephanie and Albasset, Shadi and McManus, Róisín M. and Tejera, Darío and Griep, Angelika and Santarelli, Francesco and Brosseron, Frederic and Opitz, Sabine and Stunden, James and Merten, Maximilian and Kayed, Rakez and Golenbock, Douglas Taylor and Blum, David L and Latz, Eicke and Buée, Luc and Heneka, Michael Thomas},
title = {{NLRP3 inflammasome activation drives tau pathology}},
journal = {Nature},
year = {2019},
doi = {10.1038/s41586-019-1769-z},
pmid = {31748742},
url = {https://doi.org/10.1038/s41586-019-1769-z}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record names 22 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- Loss of NLRP3 inflammasome function reduced tau hyperphosphorylation and aggregation by regulating tau kinases and phosphatases.
- Tau activated the NLRP3 inflammasome.
- Intracerebral injection of fibrillar amyloid-beta-containing brain homogenates induced tau pathology in an NLRP3-dependent manner.
- Data identify an important role of microglia and NLRP3 inflammasome activation in the pathogenesis of tauopathies.
- Data support the amyloid-cascade hypothesis in Alzheimer's disease, demonstrating that neurofibrillary tangles develop downstream of amyloid-beta-induced microglial activation.
Why it matters
Reports that activation of the NLRP3 inflammasome drives tau pathology.
How this study scored 63/100
Published in a top-tier journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on strength of evidence, so that was left out: it earned 60 of the 95 points we could judge it on, which is 63 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 10 / 10 | Tier 1 — top-tier general journal (Nature) |
| Journal's citation record | 4 / 4 | Nature: journal h-index 1,841 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | — / 5 | No evidence rating recorded — left out of this score |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 7 / 7 | Cited 1,467 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 163.0 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 6 / 6 | Cited 85.2× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 4 / 4 | Cited 644 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Michael Thomas Heneka: h-index 113 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Inserm: institution h-index 1,988 (OpenAlex) |
| Multi-centre collaboration | 2 / 3 | OpenAlex lists 9 institution(s) in 3 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 31748742) |
| Free to read | 2 / 2 | Free to read |
| Points | 60 / 95 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 60 of the 95 points we could judge it on is 63 out of 100. |
| Total | 63 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
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