Evidence map›Paper›PMID 27716675›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Tau Oligomers Associate with Inflammation in the Brain and Retina of Tauopathy Mice and in Neurodegenerative Diseases.

Ashley N Nilson, Kelsey C English, Julia E Gerson, T Barton Whittle, C Nicolas Crain, Judy Xue, Urmi Sengupta, Diana L Castillo-Carranza, Wenbo Zhang, Praveena Gupta and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed, 2 pooled it
7.6field-weighted citation impact, top 2% of its field
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

103 citing papers in PubMed, 2 syntheses or guidelines pooled it, 166 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Targeting Ferroptosis/Nrf2 Pathway Ameliorates AlClInternational journal of molecular sciences · 2025
    Article
  10. Cellular and pathological functions of tau.Nature reviews. Molecular cell biology · 2024
    Review
  11. Review
  12. Alzheimer's disease pathophysiology in the Retina.Progress in retinal and eye research · 2024
    Review
  13. Sleep deprivation soon after recovery from synthetic torpor enhances tau protein dephosphorylation in the rat brain.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024
    Article
  14. The "Hit and Run" Hypothesis for Alzheimer's Disease Pathogenesis.International journal of molecular sciences · 2024
    Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

43 more citing papers are in PubMed but not listed here.

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

11 authors at 1 institution in 1 country.

Ashley N NilsonMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
Kelsey C EnglishMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
Julia E GersonMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
T Barton WhittleDepartment of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, TX, USA.
C Nicolas CrainDepartment of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, TX, USA.
Judy XueMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
Urmi SenguptaMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
Diana L Castillo-CarranzaMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
Wenbo ZhangDepartment of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, TX, USA.
Praveena GuptaDepartment of Ophthalmology and Visual Sciences, University of Texas Medical Branch, Galveston, TX, USA.
Rakez KayedMitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
The University of Texas Medical Branch at Galveston · US

Funding

Formation and Propagation of Tau Oligomeric Strains in Alzheimer's DiseaseR01AG054025 · NIA · UNIVERSITY OF TEXAS MED BR GALVESTON · PI Rakez Kayed · 2016 to 2026
$5.8M
Mechanisms of Retinal Neuronal InjuryR01EY022694 · NEI · UNIVERSITY OF TEXAS MED BR GALVESTON · PI ZHANG, WENBO · 2012 to 2021
$3.8M
NEI NIH HHS R01 EY022694NIA NIH HHS R01 AG054025
6 · The paper itself

Abstract

It is well-established that inflammation plays an important role in Alzheimer's disease (AD) and frontotemporal lobar dementia (FTLD). Inflammation and synapse loss occur in disease prior to the formation of larger aggregates, but the contribution of tau to inflammation has not yet been thoroughly investigated. Tau pathologically aggregates to form large fibrillar structures known as tangles. However, evidence suggests that smaller soluble aggregates, called oligomers, are the most toxic species and form prior to tangles. Furthermore, tau oligomers can spread to neighboring cells and between anatomically connected brain regions. In addition, recent evidence suggests that inspecting the retina may be a window to brain pathology. We hypothesized that there is a relationship between tau oligomers and inflammation, which are hallmarks of early disease. We conducted immunofluorescence and biochemical analyses on tauopathy mice, FTLD, and AD subjects. We showed that oligomers co-localize with astrocytes, microglia, and HMGB1, a pro-inflammatory cytokine. Additionally, we show that tau oligomers are present in the retina and are associated with inflammatory cells suggesting that the retina may be a valid non-invasive biomarker for brain pathology. These results suggest that there may be a toxic relationship between tau oligomers and inflammation. Therefore, the ability of tau oligomers to spread may initiate a feed-forward cycle in which tau oligomers induce inflammation, leading to neuronal damage, and thus more inflammation. Further mechanistic studies are warranted in order to understand this relationship, which may have critical implications for improving the treatment of tauopathies.

Indexed as

Age FactorsAnimalsAstrocytesCalcium-Binding ProteinsCytokinesDisease Models, AnimalEncephalitisGene Expression RegulationGlial Fibrillary Acidic ProteinHMGB1 ProteinMiceMice, TransgenicMicrofilament ProteinsMutationNeurodegenerative DiseasesNeuronsAif1 protein, mouseCalcium-Binding ProteinsCytokinesGlial Fibrillary Acidic ProteinHMGB1 ProteinMicrofilament Proteinstau ProteinsAlzheimer’s diseasefrontotemporal lobar dementianeuroinflammationoligomerretinal degenerationtauopathytau protein

Identifiers

PMID27716675
PMCPMC5147514
OpenAlexW2528683944

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.