Evidence map›Paper›PMID 42334639›Full record

ArticleActa neuropathologica2026

CTE has multiple pathologic variants that might relate to different clinical symptom presentation.

Fatima Tuz-Zahra, Eli Hallowell, Chris Tilton, Victor E Alvarez, Nurgul Aytan, Samantha Hawkins, Jesse Mez, Michael Alosco, Ann C McKee, Yorghos Tripodis and 2 more

Abstract read
In one paragraph

Article in Acta neuropathologica, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Fatima Tuz-ZahraDepartment of Biostatistics, Boston University School of Public Health, Boston, MA, 02118, USA.
Eli HallowellDepartment of Biomedical Engineering, Boston University, Boston, MA, USA.
Chris TiltonBU Alzheimer's Disease Research and CTE Center, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Victor E AlvarezBU Alzheimer's Disease Research and CTE Center, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Nurgul AytanBU Alzheimer's Disease Research and CTE Center, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Samantha HawkinsBU Alzheimer's Disease Research and CTE Center, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Jesse MezBU Alzheimer's Disease Research and CTE Center, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Michael AloscoDepartment of Biomedical Engineering, Boston University, Boston, MA, USA.
Ann C McKeeDepartment of Pathology and Laboratory Medicine, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Yorghos TripodisDepartment of Biostatistics, Boston University School of Public Health, Boston, MA, 02118, USA.
Thor D SteinDepartment of Pathology and Laboratory Medicine, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA.
Jonathan D CherryDepartment of Pathology and Laboratory Medicine, Boston University Chobanian and Avedisian School of Medicine, Boston, MA, 02118, USA. jdcherry@bu.edu.

Funding

RL5: Research Education CoreP30AG072978 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Ann C. McKee · 2021 to 2026
$25.6M
Consequences of Exposure to Repetitive Head Impacts Across the LifespanRF1NS143015 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2025 to 2025
$4.3M
Digital Neurodegenerative Pathology After Repetitive Head ImpactsR01NS142076 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Jonathan D Cherry, Vijaya B. Kolachalama · 2025 to 2026
$1.7M
Characterization of the spatial and temporal response to tau in chronic traumatic encephalopathyR01AG090553 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Jonathan D Cherry, Adam Thomas Labadorf · 2025 to 2026
$1.6M
BLRD VA I01 BX002466NIA NIH HHS P30 AG072978NIA NIH HHS P30AG072978NIA NIH HHS R01 AG090553NIA NIH HHS R01AG090553NINDS NIH HHS R01 NS142076NINDS NIH HHS R01NS142076NINDS NIH HHS RF1 NS143015NINDS NIH HHS RF1NS143015U.S. Department of Veterans Affairs BX002466
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease found in individuals with a history of repetitive head injury (RHI) received through playing contact sports. Currently, CTE can only be diagnosed after death through the identification of perivascular neuronal hyperphosphorylated tau (pTau) pathology, found at the depth of the cortical sulcus. Although the pathognomonic lesion is found among all cases, pTau deposition is patchy and heterogeneous among individuals. To determine whether the heterogeneity of CTE masks more subtle ordering or additional disease variants, we applied the unsupervised machine learning algorithm subtype and stage inference (SuStaIn) on fully quantitative pTau density data from 26 brain regions in 207 CTE cases and 75 control cases. SuStaIn identified three distinct pathological progression subtypes: 93 cases were classified as Subtype 1 (cortical predominant) and showed dense, rapidly progressing cortical pTau akin to the classically described CTE neuropathology; Subtype 2 (cortical sparing-hippocampal enhanced) had 105 cases that exhibited a reduced cortical pTau burden that progressed slower, but also had pronounced hippocampal involvement in a CTE-specific pattern; and Subtype 3 (copathology altered) consisted of 28 older cases with higher CTE stage, was enriched for comorbid pathologies (pTDP43, Aβ, hippocampal sclerosis, and arteriolosclerosis), and had enhanced pTau in regions highly related to those additional pathologies. Clinically, impaired performance in the Functional Activities Questionnaire (FAQ) correlated with pTau regional burden and severity only in cases with Subtype 1 pathology, suggesting the enhanced cortical pTau pathology was linked to greater functional decline. Overall, these findings help characterize the heterogeneity in CTE progression, validate key pathological variants, and will be crucial for refining diagnostic criteria and advancing in-life diagnosis.

Indexed as

BrainChronic Traumatic Encephalopathytau ProteinsAgedDisease ProgressionFemaleHumansMaleMiddle AgedMAPT protein, humantau ProteinsChronic traumatic encephalopathyMachine learningNeurodegenerationpTau

Identifiers

PMID42334639
PMCPMC13290897

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.