Evidence map›Paper›PMID 25904048›Full record

ReviewBrain pathology (Zurich, Switzerland)2015

The neuropathology of chronic traumatic encephalopathy.

Ann C McKee, Thor D Stein, Patrick T Kiernan, Victor E Alvarez

Abstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 296 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
296citing papers in PubMed, 4 pooled it
–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

296 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
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  11. Water-Mediated Phosphoryl Wires Stabilize Pathological Tau Fibrils.Angewandte Chemie (International ed. in English) · 2026
    Article
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  17. Immune signaling and function in neurodegeneration.The Journal of clinical investigation · 2026
    Review
  18. Observational
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  20. Review

236 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

4 authors.

Ann C McKeeVA Boston Healthcare System, Boston University, Boston, MA; Department of Pathology and Laboratory Science, Boston University School of Medicine, Boston University, Boston, MA; Department of Neurology, Boston University School of Medicine, Boston University, Boston, MA; Boston University Alzheimer's Disease Center, Boston University, Boston, MA; Chronic Traumatic Encephalopathy Center Program, Boston University, Boston, MA.
Thor D Stein
Patrick T Kiernan
Victor E Alvarez

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
CTE and Posttraumatic Neurodegeneration: Neuropathology and Ex Vivo ImagingU01NS086659 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2014 to 2017
$6.1M
The neuropathology of mild traumatic brain injury in Alzheimer's diseaseI01CX001038 · VA · EDITH NOURSE ROGERS MEMORIAL VETERANS HOSPITAL · PI STEIN, THOR · 2015 to 2022
–
CSRD VA I01 CX001038NIA NIH HHS P30 AG013846NIA NIH HHS P30AG13846 0572063345-5NIA NIH HHS R01 AG1649NINDS NIH HHS 1U01NS086659-01NINDS NIH HHS U01 NS086659
6 · The paper itself

Abstract

Repetitive brain trauma is associated with a progressive neurological deterioration, now termed as chronic traumatic encephalopathy (CTE). Most instances of CTE occur in association with the play of sports, but CTE has also been reported in association with blast injuries and other neurotrauma. Symptoms of CTE include behavioral and mood changes, memory loss, cognitive impairment and dementia. Like many other neurodegenerative diseases, CTE is diagnosed with certainty only by neuropathological examination of brain tissue. CTE is a tauopathy characterized by the deposition of hyperphosphorylated tau (p-tau) protein as neurofibrillary tangles, astrocytic tangles and neurites in striking clusters around small blood vessels of the cortex, typically at the sulcal depths. Severely affected cases show p-tau pathology throughout the brain. Abnormalities in phosphorylated 43 kDa TAR DNA-binding protein are found in most cases of CTE; beta-amyloid is identified in 43%, associated with age. Given the importance of sports participation and physical exercise to physical and psychological health as well as disease resilience, it is critical to identify the genetic risk factors for CTE as well as to understand how other variables, such as stress, age at exposure, gender, substance abuse and other exposures, contribute to the development of CTE.

Indexed as

NeuropathologyBrainBrain Injury, ChronicDNA-Binding ProteinsHumanstau ProteinsDNA-Binding Proteinstau ProteinsAlzheimer's diseasechronic traumatic encephalopathytauopathyTDP-43traumatic brain injury

Identifiers

PMID25904048
PMCPMC4526170

What OpenQuestion holds

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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.