Evidence map›Paper›PMID 40906561›Full record

ReviewCell reports2025

Emerging roles for innate and adaptive immunity in tauopathies.

Alexis M Johnson, John R Lukens

Abstract readReview
In one paragraph

Review in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Review
  2. Neuroinflammation and Tauopathies.Molecular biology reports · 2026
    Review
  3. Article
  4. Article
  5. Immune signaling and function in neurodegeneration.The Journal of clinical investigation · 2026
    Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. 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

2 authors.

Alexis M JohnsonCenter for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, University of Virginia, Charlottesville, VA 22908, USA; Brain Immunology and Glia Graduate Training Program, University of Virginia, Charlottesville, VA 22908, USA; Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, University of Virginia, Charlottesville, VA 22903, USA.
John R LukensCenter for Brain Immunology and Glia (BIG), Department of Neuroscience, University of Virginia, Charlottesville, VA 22908, USA; Neuroscience Graduate Program, University of Virginia, Charlottesville, VA 22908, USA; Brain Immunology and Glia Graduate Training Program, University of Virginia, Charlottesville, VA 22908, USA; Harrison Family Translational Research Center in Alzheimer's and Neurodegenerative Diseases, University of Virginia, Charlottesville, VA 22903, USA. Electronic address: jrl7n@virginia.edu.

Funding

Making a case for CASS4 in Alzheimer's diseaseR01AG087406 · NIA · UNIVERSITY OF VIRGINIA · PI John R Lukens · 2024 to 2026
$1.7M
CLEC7A in microglia biology and Alzheimer's diseaseRF1AG078684 · NIA · UNIVERSITY OF VIRGINIA · PI LUKENS, JOHN R · 2023 to 2023
$1.6M
Brain, Immunology and Glia Training ProgramT32NS115657 · NINDS · UNIVERSITY OF VIRGINIA · PI Alban P Gaultier, TAJIE H. HARRIS · 2021 to 2026
$1.2M
Role of the SYK-CARD9 signaling axis in Alzheimer's diseaseR01AG071996 · NIA · UNIVERSITY OF VIRGINIA · PI LUKENS, JOHN R · 2024 to 2025
$1.1M
Exploring the Role of Microglia SYK Signaling in TauopathyF31AG089911 · NIA · UNIVERSITY OF VIRGINIA · PI JOHNSON, ALEXIS MARIE · 2024 to 2025
$77k
NIA NIH HHS F31 AG089911NIA NIH HHS R01 AG071996NIA NIH HHS R01 AG087406NIA NIH HHS RF1 AG078684NINDS NIH HHS T32 NS115657
6 · The paper itself

Abstract

Tauopathies encompass a large majority of dementia diagnoses and are characterized by toxic neuronal or glial inclusions of the microtubule-associated protein tau. Tau has a high propensity to induce prion-like spreading throughout the brain via a variety of mechanisms, making tauopathy a rapid and lethal form of neurodegeneration that currently lacks an effective therapy or cure. Tau aggregation and neuronal loss associated with this pathology are accompanied by robust neuroinflammation. Innate immune responses-particularly those involving microglial activation, altered lipid metabolism, and type I interferon signaling-have emerged as key drivers of tau hyperphosphorylation and aggregation. Recent advances also point to a significant role for the adaptive immune system in shaping tauopathy progression. This review examines the current understanding of innate immunity in tauopathies and highlights emerging evidence linking T cell responses to tauopathy progression. Last, we conclude with a discussion of potential ways in which the immune system can be harnessed to treat tauopathy.

Indexed as

Adaptive ImmunityImmunity, InnateTauopathiesAnimalsHumanstau Proteinstau Proteinsadaptive immunityAlzheimer’s diseaseCP: ImmunologyCP: Neurosciencedisease-associated microgliafrontotemporal dementiainnate immunitymicroglianeurodegenerative diseaseneuroimmunologytauopathyT cells

Identifiers

PMID40906561
PMCPMC12515501

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.