Evidence map›Paper›PMID 35410438›Full record

ArticleActa neuropathologica communications2022

Detection of astrocytic tau pathology facilitates recognition of chronic traumatic encephalopathy neuropathologic change.

Kamar E Ameen-Ali, Abigail Bretzin, Edward B Lee, Rebecca Folkerth, Lili-Naz Hazrati, Diego Iacono, C Dirk Keene, Julia Kofler, Gabor G Kovacs, Amber Nolan and 6 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
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  8. Review
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  17. Neurotrauma: 2023 Update.Free neuropathology · 2023
    Article
  18. Article
  19. Tau Pathology in Chronic Traumatic Encephalopathy is Primarily Neuronal.Journal of neuropathology and experimental neurology · 2022
    Article
  20. 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

16 authors at 18 institutions in 3 countries.

Kamar E Ameen-AliInstitute of Neuroscience and Psychology, University of Glasgow, Queen Elizabeth University Hospital, Glasgow, UK.
Abigail BretzinDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Edward B LeeDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Rebecca FolkerthOffice of Chief Medical Examiner, New York, NY, USA.
Lili-Naz HazratiDepartment of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada.
Diego IaconoDepartment of Defense/Uniformed Services, University Brain Tissue Repository and Neuropathology Program, Uniformed Services University, Bethesda, MD, USA.
C Dirk KeeneDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Julia KoflerDepartment of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
Gabor G KovacsTanz Centre for Research in Neurodegenerative Disease (CRND) and Department of Laboratory Medicine and Pathobiology, Krembil Discovery Tower, University of Toronto, 60 Leonard Ave, Toronto, ON, Canada.
Amber NolanDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Daniel P PerlDepartment of Defense/Uniformed Services, University Brain Tissue Repository and Neuropathology Program, Uniformed Services University, Bethesda, MD, USA.
David S PriemerDepartment of Defense/Uniformed Services, University Brain Tissue Repository and Neuropathology Program, Uniformed Services University, Bethesda, MD, USA.
Douglas H SmithCenter for Brain Injury and Repair, Department of Neurosurgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Douglas J WiebeDepartment of Biostatistics, Epidemiology and Informatics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
William StewartInstitute of Neuroscience and Psychology, University of Glasgow, Queen Elizabeth University Hospital, Glasgow, UK. william.stewart@glasgow.ac.uk.ORCID 0000-0003-2199-2582
CONNECT-TBI Investigators
University of Pennsylvania · USKing's College London · GBUniversity of California, San Francisco · USUniversity of Pittsburgh · USHarvard University · USHenry M. Jackson Foundation · USMassachusetts General Hospital · USQueen Elizabeth University Hospital · GBUniversity of Washington · USAllen Institute for Brain Science · USCenter for Neuroscience and Regenerative Medicine · USIcahn School of Medicine at Mount Sinai · USOffice of Chief Medical Examiner · USRush University · USSan Francisco General Hospital · USUniformed Services University of the Health Sciences · USUniversity Health Network · CAUniversity of Toronto · CA

Funding

University of Washington Alzheimer's Disease Research CenterP30AG066509 · NIA · UNIVERSITY OF WASHINGTON · PI SUMAN JAYADEV · 2020 to 2026
$29.0M
Research Education ComponentP30AG072979 · NIA · UNIVERSITY OF PENNSYLVANIA · PI DAVID A WOLK · 2021 to 2026
$24.8M
Understanding Environmental Contributions to Heterogeneity in bvFTD.P01AG066597 · NIA · UNIVERSITY OF PENNSYLVANIA · PI Corey T McMillan · 2020 to 2026
$18.8M
TRAINING PROGRAM/RESPIRATORY NEUROBIOLOGY AND SLEEPT32HL007713 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI PACK, ALLAN I · 1992 to 2022
$11.9M
Data Coordinating CoreU54NS115322 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI SMITH, DOUGLAS HAMILTON · 2019 to 2023
$9.2M
TRANSGENIC MODELS OF HUNTINGTONS DISEASER01NS038144 · NINDS · JOHNS HOPKINS UNIVERSITY · PI ROSS, CHRISTOPHER A · 1999 to 2006
$2.6M
Cortical Somatostatin Interneuron Dysfunction after Trauma: Role in Cognitive FlexibilityK08NS114170 · NINDS · UNIVERSITY OF WASHINGTON · PI NOLAN, AMBER L · 2019 to 2023
$1.0M
NHLBI NIH HHS T32 HL007713NIA NIH HHS P01 AG066597NIA NIH HHS P30 AG066509NIA NIH HHS P30 AG072979NINDS NIH HHS K08 NS114170NINDS NIH HHS R01 NS038144NINDS NIH HHS U54 NS115322
6 · The paper itself

Abstract

Traumatic brain injury (TBI) is associated with the development of a range of neurodegenerative pathologies, including chronic traumatic encephalopathy (CTE). Current consensus diagnostic criteria define the pathognomonic cortical lesion of CTE neuropathologic change (CTE-NC) as a patchy deposition of hyperphosphorylated tau in neurons, with or without glial tau in thorn-shaped astrocytes, typically towards the depths of sulci and clustered around small blood vessels. Nevertheless, although incorporated into consensus diagnostic criteria, the contribution of the individual cellular components to identification of CTE-NC has not been formally evaluated. To address this, from the Glasgow TBI Archive, cortical tissue blocks were selected from consecutive brain donations from contact sports athletes in which there was known to be either CTE-NC (n = 12) or Alzheimer's disease neuropathologic change  (n = 4). From these tissue blocks, adjacent tissue sections were stained for tau antibodies selected to reveal either solely neuronal pathology (3R tau; GT-38) or mixed neuronal and astroglial pathologies (4R tau; PHF-1). These stained sections were then randomised and independently assessed by a panel of expert neuropathologists, blind to patient clinical history and primary antibody applied to each section, who were asked to record whether CTE-NC was present. Results demonstrate that, in sections stained for either 4R tau or PHF-1, consensus recognition of CTE-NC was high. In contrast, recognition of CTE-NC in sections stained for 3R tau or GT-38 was poor; in the former no better than chance. Our observations demonstrate that the presence of both neuronal and astroglial tau pathologies facilitates detection of CTE-NC, with its detection less consistent when neuronal tau pathology alone is visible. The combination of both glial and neuronal pathologies, therefore, may be required for detection of CTE-NC.

Indexed as

Alzheimer DiseaseBrain Injuries, TraumaticChronic Traumatic EncephalopathyAstrocytesBrainHumansNeuropathologytau Proteinstau ProteinsAging-related tau astrogliopathyChronic traumatic encephalopathyNeurodegenerationTauTraumatic brain injury

Identifiers

PMID35410438
PMCPMC8996534
OpenAlexW4223587132

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.