Evidence map›Paper›PMID 30564964›Full record

ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2019

Cortical degeneration in chronic traumatic encephalopathy and Alzheimer's disease neuropathologic change.

Richard A Armstrong, Ann C McKee, Thor D Stein, Victor E Alvarez, Nigel J Cairns

Open access · hybridAbstract read
In one paragraph

Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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

5 authors at 3 institutions in 2 countries.

Richard A ArmstrongVision Sciences, Aston University, Birmingham, B4 7ET, UK. R.A.Armstrong@aston.ac.uk.ORCID http://orcid.org/0000-0002-5046-3199
Ann C McKeeVA Boston HealthCare System, Boston, MA, 02130, USA.
Thor D SteinDepartment of Pathology & Laboratory Medicine, Boston University School of Medicine, Boston, MA, 02118, USA.
Victor E AlvarezDepartment of Neurology, Boston University School of Medicine, Boston, MA, 02118, USA.
Nigel J CairnsDepartments of Neurology and Pathology & Immunology, Washington University School of Medicine, Saint Louis, MO, 63110, USA.
Boston University · USAston University · GBWashington University in St. Louis · US

Funding

Smartphone-Based "Burst" Cognitive AssessmentsP01AG003991 · NIA · WASHINGTON UNIVERSITY · PI Tammie Lee Smith Benzinger · 1985 to 2026
$69.5M
WASHINGTON UNIVERSITY ALZHEIMERS DISEASE RESEARCH CENTERP50AG005681 · NIA · WASHINGTON UNIVERSITY · PI MORRIS, JOHN · 1985 to 2019
$52.1M
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
NIA NIH HHS P01 AG003991NIA NIH HHS P30 AG013846NIA NIH HHS P50 AG005681NINDS NIH HHS 1UO1NS086659-01NINDS NIH HHS U01 NS086659
6 · The paper itself

Abstract

objectivesAn observational study to compare the laminar distributions in frontal and temporal cortex of the tau-immunoreactive pathologies in chronic traumatic encephalopathy (CTE) and Alzheimer's disease neuropathologic change (ADNC). PATIENTS: Post-mortem material of (1) four cases of CTE without ADNC, (2) seven cases of CTE with ADNC (CTE/ADNC), and (3) seven cases of ADNC alone.

resultsIn CTE and CTE/ADNC, neurofibrillary tangles (NFT), neuropil threads (NT), and dot-like grains (DLG) were distributed either in upper cortex or across all layers. Low densities of astrocytic tangles (AT) and abnormally enlarged neurons (EN) were not localized to any specific layer. Surviving neurons exhibited peaks of density in both upper and lower cortex, and vacuole density was greatest in superficial layers. In ADNC, neuritic plaques (NP) were more frequent, AT rare, NFT and NT were more widely distributed, NT affected lower layers more frequently, and surviving neurons were less frequently bimodal than in CTE and CTE/ADNC.

conclusionTau pathology in CTE and CTE/ADNC consistently affected the upper cortex but was more widely distributed in ADNC. The presence of CTE may encourage the development of ADNC pathology later in the course of the disease.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseCerebral CortexChi-Square DistributionChronic Traumatic EncephalopathyDiagnosisFemaleHumansMaleMiddle AgedNeurofibrillary TanglesNeuronsPlaque, AmyloidAlzheimer’s disease neuropathologic change (ADNC)Chronic traumatic encephalopathy (CTE)Laminar distributionTauopathy

Identifiers

PMID30564964
PMCPMC6433808
OpenAlexW2903919200

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.