Evidence map›Paper›PMID 34019156›Full record

ArticleActa neuropathologica2021

Altered oligodendroglia and astroglia in chronic traumatic encephalopathy.

K Blake Chancellor, Sarah E Chancellor, Joseph E Duke-Cohan, Bertrand R Huber, Thor D Stein, Victor E Alvarez, Benjamin W Okaty, Susan M Dymecki, Ann C McKee

Open access · hybridAbstract read
In one paragraph

Article in Acta neuropathologica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Brain regional susceptibility to tauopathy in individuals at risk for chronic traumatic encephalopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  18. Evaluation of Tau Radiotracers in Chronic Traumatic Encephalopathy.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2023
    Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

K Blake Chancellor *Department of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA.
Sarah E Chancellor *Alzheimer's Disease Research and Chronic Traumatic Encephalopathy Center, Boston University School of Medicine, 72 East Concord Street, B-7800, Boston, MA, 02118, USA.
Joseph E Duke-CohanDepartment of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA.
Bertrand R HuberAlzheimer's Disease Research and Chronic Traumatic Encephalopathy Center, Boston University School of Medicine, 72 East Concord Street, B-7800, Boston, MA, 02118, USA.
Thor D SteinAlzheimer's Disease Research and Chronic Traumatic Encephalopathy Center, Boston University School of Medicine, 72 East Concord Street, B-7800, Boston, MA, 02118, USA.
Victor E AlvarezAlzheimer's Disease Research and Chronic Traumatic Encephalopathy Center, Boston University School of Medicine, 72 East Concord Street, B-7800, Boston, MA, 02118, USA.
Benjamin W OkatyDepartment of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA.
Susan M DymeckiDepartment of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA.
Ann C McKeeAlzheimer's Disease Research and Chronic Traumatic Encephalopathy Center, Boston University School of Medicine, 72 East Concord Street, B-7800, Boston, MA, 02118, USA. amckee@bu.edu.ORCID 0000-0003-2961-7488
Boston University · USHarvard University · US

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
Neuropathology CoreP30AG013854 · NIA · NORTHWESTERN UNIVERSITY AT CHICAGO · PI BIGIO, EILEEN H. · 1996 to 2020
$28.9M
Toward better characterization and clinical trial readiness for targeting neuropsychiatric manifestations in PTEN pathogenic variantsU54NS092090 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI Joseph D. Buxbaum · 2014 to 2026
$20.1M
Traumatic Brain Injury and Repetitive Head Impacts: Contributions to AD/ADRD and CTE Neuropathology and Resulting Clinical SyndromesU54NS115266 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2019 to 2023
$10.3M
Genetic Analysis and Manipulation Core (GAEC)P50HD105351 · NICHD · BOSTON CHILDREN'S HOSPITAL · PI SCOTT Loren POMEROY, MUSTAFA SAHIN · 2021 to 2026
$9.4M
CTE and Posttraumatic Neurodegeneration: Neuropathology and Ex Vivo ImagingU01NS086659 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2014 to 2017
$6.1M
Tau Pathology in CTE vs. Alzheimer's Disease: Microvasculopathy and NeuroinflammationRF1AG057902 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2017 to 2017
$4.1M
NIA NIH HHS P30 AG013846NIA NIH HHS P30 AG013854NIA NIH HHS RF1 AG057902NICHD NIH HHS P50 HD105351NINDS NIH HHS U01 NS086659NINDS NIH HHS U54 NS092090NINDS NIH HHS U54 NS115266
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a progressive tauopathy found in contact sport athletes, military veterans, and others exposed to repetitive head impacts. White matter rarefaction and axonal loss have been reported in CTE but have not been characterized on a molecular or cellular level. Here, we present RNA sequencing profiles of cell nuclei from postmortem dorsolateral frontal white matter from eight individuals with neuropathologically confirmed CTE and eight age- and sex-matched controls. Analyzing these profiles using unbiased clustering approaches, we identified eighteen transcriptomically distinct cell groups (clusters), reflecting cell types and/or cell states, of which a subset showed differences between CTE and control tissue. Independent in situ methods applied on tissue sections adjacent to that used in the single-nucleus RNA-seq work yielded similar findings. Oligodendrocytes were found to be most severely affected in the CTE white matter samples; they were diminished in number and altered in relative proportions across subtype clusters. Further, the CTE-enriched oligodendrocyte population showed greater abundance of transcripts relevant to iron metabolism and cellular stress response. CTE tissue also demonstrated excessive iron accumulation histologically. In astrocytes, total cell numbers were indistinguishable between CTE and control samples, but transcripts associated with neuroinflammation were elevated in the CTE astrocyte groups compared to controls. These results demonstrate specific molecular and cellular differences in CTE oligodendrocytes and astrocytes and suggest that white matter alterations are a critical aspect of CTE neurodegeneration.

Indexed as

AgedAstrocytesAthletesAthletic InjuriesChronic Traumatic EncephalopathyHumansMaleMiddle AgedNeuroinflammatory DiseasesOligodendrogliaSportsTauopathiestau ProteinsWhite Mattertau ProteinsAstrocytesChronic traumatic encephalopathyNeurodegenerationOligodendrocytesSingle-nucleus transcriptomicsWhite matter

Identifiers

PMID34019156
PMCPMC8270845
OpenAlexW3162215487

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.