Evidence map›Paper›PMID 25943889›Full record

ArticleActa neuropathologica2015

Beta-amyloid deposition in chronic traumatic encephalopathy.

Thor D Stein, Philip H Montenigro, Victor E Alvarez, Weiming Xia, John F Crary, Yorghos Tripodis, Daniel H Daneshvar, Jesse Mez, Todd Solomon, Gaoyuan Meng and 13 more

Open access · greenAbstract read
In one paragraph

Article in Acta neuropathologica, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 151 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
151citing papers in PubMed, 2 pooled it
19.6field-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

151 citing papers in PubMed, 2 syntheses or guidelines pooled it, 286 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Review
  6. Article
  7. Observational
  8. Tau catalyzes amyloid-β aggregation and toxicity in a polymorph-dependent manner.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Review

91 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

23 authors at 3 institutions in 1 country.

Thor D SteinVA Boston Healthcare System, Boston, MA, 02130, USA, tdstein@bu.edu.
Philip H Montenigro
Victor E Alvarez
Weiming Xia
John F Crary
Yorghos Tripodis
Daniel H Daneshvar
Jesse Mez
Todd Solomon
Gaoyuan Meng
Caroline A Kubilus
Kerry A Cormier
Steven Meng
Katharine Babcock
Patrick Kiernan
Lauren Murphy
Christopher J Nowinski
Brett Martin
Diane Dixon
Robert A Stern
Robert C Cantu
Neil W Kowall
Ann C McKee
Boston University · USVA Boston Healthcare System · USIcahn School of Medicine at Mount Sinai · 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
Mechanisms of Age-Related TauopathyR01NS095252 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI John Fonda Crary · 2015 to 2026
$3.4M
Genetic and Neuropsychological Heterogeneity in Alzheimer's DiseaseK23AG046377 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MEZ, JESSE BENJAMIN · 2014 to 2018
$639k
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 K23 AG046377NIA NIH HHS P30 AG013846NIA NIH HHS P30AG13846NINDS NIH HHS R01 NS095252NINDS NIH HHS U01 NS086659NINDS NIH HHS U01NS086659-01
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid β peptide (Aβ) levels, the extent of Aβ deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that Aβ deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Aβ deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Aβ deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p < 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Aβ plaques and those without. Aβ deposition was significantly associated with the presence of the APOE ε4 allele (p = 0.035), older age at symptom onset (p < 0.001), and older age at death (p < 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (β = 2.43, p = 0.018), co-morbid Lewy body disease (OR = 5.01, p = 0.009), and dementia (OR = 4.45, p = 0.012). A subset of subjects met the diagnostic criteria for both CTE and AD, and in these subjects both Aβ plaques and total levels of Aβ1-40 were increased at the depths of the cortical sulcus compared to the gyral crests. Overall, these findings suggest that Aβ deposition is altered and accelerated in a cohort of CTE subjects compared to normal aging and that Aβ is associated with both pathological and clinical progression of CTE independent of age.

Indexed as

AdultAgedAged, 80 and overAge FactorsAmyloid beta-PeptidesApolipoprotein E4AthletesAthletic InjuriesBrainBrain Injury, ChronicCohort StudiesComorbidityHumansMiddle AgedNeurodegenerative DiseasesPlaque, AmyloidAmyloid beta-PeptidesApolipoprotein E4MAPT protein, humantau Proteins

Identifiers

PMID25943889
PMCPMC4529056
OpenAlexW856139224

What OpenQuestion holds

Textmetadata
LicenceTDM
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.