Evidence map›Paper›PMID 33527898›Full record

ArticleeLife2021

Seizures are a druggable mechanistic link between TBI and subsequent tauopathy.

Hadeel Alyenbaawi, Richard Kanyo, Laszlo F Locskai, Razieh Kamali-Jamil, Michèle G DuVal, Qing Bai, Holger Wille, Edward A Burton, W Ted Allison

Open access · goldAbstract read
In one paragraph

Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

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  11. Acute Treatment with the M-Channel (KNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Article
  12. Abusive Head Trauma Animal Models: Focus on Biomarkers.International journal of molecular sciences · 2023
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 3 countries.

Hadeel AlyenbaawiCentre for Prions & Protein Folding Disease, University of Alberta, Edmonton, Canada.
Richard KanyoCentre for Prions & Protein Folding Disease, University of Alberta, Edmonton, Canada.
Laszlo F LocskaiCentre for Prions & Protein Folding Disease, University of Alberta, Edmonton, Canada.
Razieh Kamali-JamilCentre for Prions & Protein Folding Disease, University of Alberta, Edmonton, Canada.
Michèle G DuValDepartment of Biological Sciences, University of Alberta, Edmonton, Canada.ORCID 0000-0001-6975-8117
Qing BaiDepartment of Neurology, University of Pittsburgh, Pittsburgh, United States.
Holger WilleCentre for Prions & Protein Folding Disease, University of Alberta, Edmonton, Canada.ORCID 0000-0001-5102-8706
Edward A BurtonDepartment of Neurology, University of Pittsburgh, Pittsburgh, United States.ORCID 0000-0002-8072-4636
W Ted AllisonCentre for Prions & Protein Folding Disease, University of Alberta, Edmonton, Canada.ORCID 0000-0002-8461-4864
University of Alberta · CAUniversity of Pittsburgh · US

Funding

Development of Zebrafish Taupoathy Models for Translational ResearchR21NS080881 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BURTON, EDWARD ALAN · 2013 to 2014
$419k
Role of BET proteins in neuroinflammation in tauopathyI01BX003168 · VA · VETERANS HEALTH ADMINISTRATION · PI Edward Alan Burton · 2017 to 2026
–
BLRD VA I01 BX003168CIHRNINDS NIH HHS R21 NS080881
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is a prominent risk factor for dementias including tauopathies like chronic traumatic encephalopathy (CTE). The mechanisms that promote prion-like spreading of Tau aggregates after TBI are not fully understood, in part due to lack of tractable animal models. Here, we test the putative role of seizures in promoting the spread of tauopathy. We introduce 'tauopathy reporter' zebrafish expressing a genetically encoded fluorescent Tau biosensor that reliably reports accumulation of human Tau species when seeded via intraventricular brain injections. Subjecting zebrafish larvae to a novel TBI paradigm produced various TBI features including cell death, post-traumatic seizures, and Tau inclusions. Bath application of dynamin inhibitors or anticonvulsant drugs rescued TBI-induced tauopathy and cell death. These data suggest a role for seizure activity in the prion-like seeding and spreading of tauopathy following TBI. Further work is warranted regarding anti-convulsants that dampen post-traumatic seizures as a route to moderating subsequent tauopathy.

Indexed as

AnimalsAnimals, Genetically ModifiedAnticonvulsantsBrain Injuries, TraumaticCell DeathDynaminsGreen Fluorescent ProteinsLarvaMiceSeizuresTauopathiestau ProteinsZebrafishAnticonvulsantsDynaminsGreen Fluorescent Proteinstau Proteinsanti-epilepticsepilepsyneuroscienceneurotraumapost-traumatic seizurestauopathytraumatic brain injuryzebrafish

Identifiers

PMID33527898
PMCPMC7853719
OpenAlexW3126875969

What OpenQuestion holds

Textmetadata
LicenceCC0
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.