Evidence map›Paper›PMID 42380200›Full record

ArticleNature communications2026

Select microbial metabolites promote tau aggregation in a murine tauopathy model.

Sabeen A Kazmi, Franciscus Chandra, Michael Wasney, Jenny Cheng, Gregory R Lum, Malvika Iyer, Daria Di Blasi, Adriana N Espinoza, Arlene Lopez-Romero, Xia Yang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Sabeen A KazmiDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA. sak14@g.ucla.edu.ORCID http://orcid.org/0000-0002-3913-6170
Franciscus ChandraDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.
Michael WasneyDepartment of Ecology and Evolutionary Biology, University of California, Los Angeles, Los Angeles, CA, USA.
Jenny ChengDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.
Gregory R LumDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.
Malvika IyerDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.
Daria Di BlasiDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.
Adriana N EspinozaUCLA Goodman-Luskin Microbiome Center, Vatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, Los Angeles, CA, USA.
Arlene Lopez-RomeroUCLA Goodman-Luskin Microbiome Center, Vatche and Tamar Manoukian Division of Digestive Diseases, Department of Medicine, David Geffen School of Medicine, Los Angeles, CA, USA.ORCID http://orcid.org/0009-0005-1141-713X
Xia YangDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0002-3971-038X
Nandita GarudDepartment of Ecology and Evolutionary Biology, University of California, Los Angeles, Los Angeles, CA, USA.ORCID http://orcid.org/0000-0003-4217-4407
Elaine Y HsiaoDepartment of Integrative Biology and Physiology, University of California, Los Angeles, Los Angeles, CA, USA. ehsiao@g.ucla.edu.ORCID http://orcid.org/0000-0002-1633-588X

Funding

Silicon Valley Community Foundation (SVCF) 2018-191860
6 · The paper itself

Abstract

The gut microbiome is emerging as a modifier of risk for neurodegenerative diseases, but underlying mechanisms remain poorly understood. Here, we show that the hTau.P301S mouse model for progressive tauopathy develops alterations in the composition and function of the gut microbiome that are not recapitulated in amyloid-based 5xFAD or 3xTg models for Alzheimer's disease. Disrupting the gut microbiome via chronic antibiotic treatment exacerbates cognitive deficits and tau pathology in hTau.P301S mice, demonstrating a causal influence of the microbiome on tau-driven disease progression. This corresponds with widespread alterations in microbiome-dependent metabolites in the sera and brains of hTau.P301S mice, including subsets that correlate with the severity of tau pathology. By screening against tau biosensor cells, we identify select microbial metabolites-trimethylamine-N-oxide, 3-indoxyl sulfate, phenol sulfate, thymidine, and 2'deoxyuridine-that promote tau seeding and aggregation. Systemic administration of these metabolites worsens cognitive impairment and tau pathology in hTau.P301S mice. These findings establish a mechanistic link between the gut microbiome, serum and brain metabolites, as well as tau aggregation, suggesting that select microbial metabolites could potentially serve as therapeutic targets for tau-driven diseases.

Indexed as

Gastrointestinal MicrobiomeProtein Aggregation, PathologicalTauopathiestau ProteinsAlzheimer DiseaseAnimalsBrainDisease Models, AnimalFemaleHumansMaleMiceMice, Transgenictau Proteins

Identifiers

PMID42380200
PMCPMC13458332

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.