Evidence map›Paper›PMID 41726919›Full record

ArticlebioRxiv : the preprint server for biology2026

Proteomic Analysis of Human Chronic Traumatic Encephalopathy Brain Implicates Proteasome and Ribosome Dysfunction in Disease Progression.

Helen E Pennington, Dillon Shapiro, Jenny Empawi, Nurgul Aytan, Victor Alvarez, Jessie Mez, Michael L Alosco, Xiaoling Zhang, Ann C McKee, Thor D Stein and 2 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 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

5 · Who and what money

Authors and funding

12 authors.

Helen E PenningtonBioinformatics Program, Boston University.ORCID 0009-0004-6534-5859
Dillon ShapiroBoston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine.
Jenny EmpawiBoston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine.ORCID 0009-0007-5736-6934
Nurgul AytanVA Boston Healthcare System, U.S. Department of Veteran Affairs, Boston.
Victor AlvarezVA Bedford Healthcare System, Bedford, MA.
Jessie MezBoston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine.ORCID 0000-0003-1438-5442
Michael L AloscoBoston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine.ORCID 0000-0002-8113-8428
Xiaoling ZhangBoston University Alzheimer's Disease Research Center and CTE Centers, Department of Neurology, Boston University School of Medicine.ORCID 0000-0001-8237-1857
Ann C McKeeVA Bedford Healthcare System, Bedford, MA.ORCID 0000-0003-2961-7488
Thor D SteinVA Boston Healthcare System, U.S. Department of Veteran Affairs, Boston.ORCID 0000-0001-6954-4477
Jonathan D CherryVA Boston Healthcare System, U.S. Department of Veteran Affairs, Boston.ORCID 0000-0002-1257-981X
Adam LabadorfBioinformatics Program, Boston University.ORCID 0000-0002-0753-8992

Funding

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
Predoctoral Training in Bioinformatics and Computational BiologyT32GM150533 · NIGMS · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI GARY E. BENSON, Daniel Segre · 2023 to 2026
$1.3M
NIA NIH HHS R01 AG090553NIGMS NIH HHS T32 GM150533
6 · The paper itself

Abstract

Chronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease associated with repeated head injuries (RHI) commonly experienced by contact sport athletes, military personnel, and domestic abuse victims. Despite growing recognition of CTE, the molecular mechanisms underlying disease progression remain poorly understood. This study aims to identify proteomic alterations associated with CTE pathology and clinical features to elucidate key biological pathways involved in disease pathogenesis. SomaScan 7k high-throughput proteomics was performed on 204 dorsolateral prefrontal cortex samples from the Boston University CTE Center Brain Bank. We identified differentially expressed proteins associated with CTE, hyperphosphorylated tau (ptau) pathology, duration of contact sports play, dementia status, and Cognitive Difficulty Scale (CDS) scores. Gene set enrichment analysis revealed that proteasome subunit proteins and related pathways were strongly associated with CTE progression and correlated with years of contact sports play. Reduction in ribosomal proteins and pathways was closely associated with ptau burden. Additionally, multiple models demonstrated significant alterations in MAPK-related cell signaling pathways. These findings advance our understanding of CTE progression and identify mechanisms correlated with key pathological features of the disease. Validation of these results could inform the development of diagnostics and treatments for CTE.

Indexed as

CTENeurodegenerationProteomicsRepetitive head impactsTauopathy

Identifiers

PMID41726919
PMCPMC12918859

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.