Evidence map›Paper›PMID 24423082›Full record

ReviewAlzheimer's research & therapy2014

Chronic traumatic encephalopathy: a spectrum of neuropathological changes following repetitive brain trauma in athletes and military personnel.

Thor D Stein, Victor E Alvarez, Ann C McKee

Open access · goldAbstract readReview
In one paragraph

Review in Alzheimer's research & therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
113citing papers in PubMed, 1 pooled it
22.5field-weighted citation impact, top 1% 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

113 citing papers in PubMed, 1 synthesis or guideline pooled it, 262 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Brain regional susceptibility to tauopathy in individuals at risk for chronic traumatic encephalopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Article
  8. Review
  9. Forensic neuroimaging in childhood abduction, rape and murder case and trial outcome.Psychiatry, psychology, and law : an interdisciplinary journal of the Australian and New Zealand Association of Psychiatry, Psychology and Law · 2026
    Article
  10. Article
  11. Article
  12. Review
  13. Article
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  16. Article
  17. Article
  18. Cerebrovascular remodeling in aging and neurodegenerative disease progression.Frontiers in bioengineering and biotechnology · 2025
    Article
  19. Review
  20. Article

53 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

3 authors at 2 institutions in 1 country.

Thor D SteinVA Boston HealthCare System, 150 South Huntington Avenue, Boston, MA 02130, USA ; Bedford VA Medical Center, 200 Springs Road, Bedford, MA 01730, USA ; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA ; Department of Neurology, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA ; Alzheimer Disease Center, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA.
Victor E AlvarezBedford VA Medical Center, 200 Springs Road, Bedford, MA 01730, USA ; Department of Neurology, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA ; Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA.
Ann C McKeeVA Boston HealthCare System, 150 South Huntington Avenue, Boston, MA 02130, USA ; Department of Pathology and Laboratory Medicine, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA ; Department of Neurology, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA ; Alzheimer Disease Center, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA ; Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, 72 East Concord Street, Boston, MA 02118, USA.
VA Boston Healthcare System · USBedford VA Research Corporation · US

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 AG013846NINDS NIH HHS U01 NS086659
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease that occurs in association with repetitive traumatic brain injury experienced in sport and military service. In most instances, the clinical symptoms of the disease begin after a long period of latency ranging from several years to several decades. The initial symptoms are typically insidious, consisting of irritability, impulsivity, aggression, depression, short-term memory loss and heightened suicidality. The symptoms progress slowly over decades to include cognitive deficits and dementia. The pathology of CTE is characterized by the accumulation of phosphorylated tau protein in neurons and astrocytes in a pattern that is unique from other tauopathies, including Alzheimer's disease. The hyperphosphorylated tau abnormalities begin focally, as perivascular neurofibrillary tangles and neurites at the depths of the cerebral sulci, and then spread to involve superficial layers of adjacent cortex before becoming a widespread degeneration affecting medial temporal lobe structures, diencephalon and brainstem. Most instances of CTE (>85% of cases) show abnormal accumulations of phosphorylated 43 kDa TAR DNA binding protein that are partially colocalized with phosphorylated tau protein. As CTE is characterized pathologically by frontal and temporal lobe atrophy, by abnormal deposits of phosphorylated tau and by 43 kDa TAR DNA binding protein and is associated clinically with behavioral and personality changes, as well as cognitive impairments, CTE is increasingly categorized as an acquired frontotemporal lobar degeneration. Currently, some of the greatest challenges are that CTE cannot be diagnosed during life and the incidence and prevalence of the disorder remain uncertain. Furthermore, the contribution of age, gender, genetics, stress, alcohol and substance abuse to the development of CTE remains to be determined.

Identifiers

PMID24423082
PMCPMC3979082
OpenAlexW2124200927

What OpenQuestion holds

Textmetadata
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.