Evidence map›Paper›PMID 38407651›Full record

ArticleActa neuropathologica2024

Cortical-sparing chronic traumatic encephalopathy (CSCTE): a distinct subtype of CTE.

Abigail Alexander, Victor E Alvarez, Bertrand R Huber, Michael L Alosco, Jesse Mez, Yorghos Tripodis, Raymond Nicks, Douglas I Katz, Brigid Dwyer, Daniel H Daneshvar and 11 more

Open access · greenAbstract read
In one paragraph

Article in Acta neuropathologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
3.9field-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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
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  3. Article
  4. Review
  5. Article
  6. Observational
  7. Article
  8. Molecular neurodegeneration · 2025
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  10. Article
  11. Review
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

21 authors at 4 institutions in 1 country.

Abigail AlexanderDivision of Neuropathology, Lifespan Academic Medical Center, The Warren Alpert Medical School, Brown University, Providence, RI, USA.
Victor E AlvarezBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Bertrand R HuberBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Michael L AloscoBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Jesse MezBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Yorghos TripodisBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Raymond NicksBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Douglas I KatzDepartment of Neurology, Boston University, Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Brigid DwyerDepartment of Neurology, Boston University, Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Daniel H DaneshvarDepartment of Physical Medicine and Rehabilitation, Harvard Medical School, Boston, MA, USA.
Brett MartinBiostatistics and Epidemiology Data Analytics Center, Boston University School of Public Health, Boston, MA, USA.
Joseph PalmisanoBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Lee E GoldsteinBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
John F CraryDepartment of Pathology, Nash Family Department of Neuroscience, Department of Artificial Intelligence and Human Health, Ronald M. Loeb Center for Alzheimer's Disease, Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
Christopher NowinskiBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Robert C CantuBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Neil W KowallBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Robert A SternBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Ivana DelalleDivision of Neuropathology, Lifespan Academic Medical Center, The Warren Alpert Medical School, Brown University, Providence, RI, USA.
Ann C McKeeBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA.
Thor D SteinBoston University Alzheimer's Disease Research Center and CTE Center, Department of Neurology, Boston University Chobanian & Avedisian School of Medicine, Boston, MA, USA. tdstein@bu.edu.ORCID 0000-0001-6954-4477
Boston University · USBrown University · USAllen Institute for Brain Science · USHarvard University · US

Funding

RL5: Research Education CoreP30AG072978 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Thor Stein · 2021 to 2026
$25.6M
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
CTE and Posttraumatic Neurodegeneration: Neuropathology and Ex Vivo ImagingU01NS086659 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2014 to 2017
$6.1M
The Contribution of Age-Related Taupahtoies to Alzheimer's Disease-SupplementR01AG062348 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI CRARY, JOHN FONDA, DICKSON, DENNIS WILLIAM · 2018 to 2022
$4.5M
The Contribution of Age-Related Tauopathies to Alzheimer's DiseaseRF1AG062348 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI John Fonda Crary, DENNIS WILLIAM DICKSON · 2023 to 2026
$4.0M
Cerebrovascular Remodeling and Neurodegenerative Changes in Alzheimer's DiseaseR01AG075876 · NIA · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI Thor Stein, JOSEPH ZAIA · 2022 to 2026
$3.9M
Late Pathologies of Exposure to Repetitive Head Impacts from Contact Sports: White Matter and Vascular Contributions to Cognitive Impairment, Dementia, and Neuropsychiatric SymptomsRF1NS122854 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ALOSCO, MICHAEL, MCKEE, ANN C. · 2021 to 2021
$2.3M
Blood Biomarker Development and Validation in Chronic Traumatic Encephalopathy and Alzheimer's Disease and Alzheimer's Disease Related DementiasRF1NS132290 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ALOSCO, MICHAEL, STEIN, THOR · 2023 to 2023
$1.9M
Late Pathologies of Exposure to Repetitive Head Impacts from Contact Sports: White Matter and Vascular Contributions to Cognitive Impairment, Dementia, and Neuropsychiatric SymptomsR01NS122854 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ALOSCO, MICHAEL, MCKEE, ANN C. · 2024 to 2025
$1.6M
Repetitive Head Impact Exposure and Later-Life White Matter Signal Abnormalities: An Investigation in Former NFL Players, Subjects with Alzheimer's Disease, and Cognitively Normal ControlsK23NS102399 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI ALOSCO, MICHAEL · 2018 to 2022
$793k
VA Biorepository Brain BankI01BX002466 · VA · VA BOSTON HEALTH CARE SYSTEM · PI Ann C. McKee, Haining Zhu · 2014 to 2026
–
The neuropathology of mild traumatic brain injury in Alzheimer's diseaseI01BX005933 · VA · EDITH NOURSE ROGERS MEMORIAL VETERANS HOSPITAL · PI Thor Stein · 2023 to 2026
–
Alzheimer's Association NIRG-305779Alzheimer's Association NIRG-362697BLRD VA I01 BX002466BLRD VA I01 BX005161BLRD VA I01 BX005933NIA NIH HHS P30 AG072978NIA NIH HHS R01 AG062348NIA NIH HHS R01 AG075876NIA NIH HHS RF1 AG062348NINDS NIH HHS K23 NS102399NINDS NIH HHS K23NS102399NINDS NIH HHS R01 NS122854NINDS NIH HHS RF1 NS122854NINDS NIH HHS RF1NS122854NINDS NIH HHS RF1 NS132290NINDS NIH HHS U01 NS086659NINDS NIH HHS U01NS086659NINDS NIH HHS U54 NS115266NINDS NIH HHS U54NS115266
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease caused by repetitive head impacts (RHI) and pathologically defined as neuronal phosphorylated tau aggregates around small blood vessels and concentrated at sulcal depths. Cross-sectional studies suggest that tau inclusions follow a stereotyped pattern that begins in the neocortex in low stage disease, followed by involvement of the medial temporal lobe and subcortical regions with significant neocortical burden in high stage CTE. Here, we define a subset of brain donors with high stage CTE and with a low overall cortical burden of tau inclusions (mean semiquantitative value ≤1) and classify them as cortical-sparing CTE (CSCTE). Of 620 brain donors with pathologically diagnosed CTE, 66 (11%) met criteria for CSCTE. Compared to typical high stage CTE, those with CSCTE had a similar age at death and years of contact sports participation and were less likely to carry apolipoprotein ε4 (p < 0.05). CSCTE had less overall tau pathology severity, but a proportional increase of disease burden in medial temporal lobe and brainstem regions compared to the neocortex (p's < 0.001). CSCTE also had lower prevalence of comorbid neurodegenerative disease. Clinically, CSCTE participants were less likely to have dementia (p =  0.023) and had less severe cognitive difficulties (as reported by informants using the Functional Activities Questionnaire (FAQ); p < 0.001, meta-cognitional index T score; p = 0.002 and Cognitive Difficulties Scale (CDS); p < 0.001,) but had an earlier onset age of behavioral (p = 0.006) and Parkinsonian motor (p = 0.013) symptoms when compared to typical high stage CTE. Other comorbid tauopathies likely contributed in part to these differences: when cases with concurrent Alzheimer dementia or frontal temporal lobar degeneration with tau pathology were excluded, differences were largely retained, but only remained significant for FAQ (p = 0.042), meta-cognition index T score (p = 0.014) and age of Parkinsonian motor symptom onset (p = 0.046). Overall, CSCTE appears to be a distinct subtype of high stage CTE with relatively greater involvement of subcortical and brainstem regions and less severe cognitive symptoms.

Indexed as

Alzheimer DiseaseChronic Traumatic EncephalopathyNeurodegenerative DiseasesBrainCross-Sectional StudiesHumansChronic traumatic encephalopathyNeurodegenerative diseaseRepetitive head impactsTraumatic brain injury

Identifiers

PMID38407651
PMCPMC11348287
OpenAlexW4392162625

What OpenQuestion holds

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Registered trials

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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.