Evidence map›Paper›PMID 41957675›Full record

ArticleActa neuropathologica communications2026

Meningeal and infiltrating T-cells are associated with repetitive head trauma and tau-mediated neurodegeneration in chronic traumatic encephalopathy.

Samantha M Calderazzo, Morgane L M D Butler, Kerry Breen, Hersh Kanner, Yorghos Tripodis, Thor D Stein, David M Holtzman, Jonathan D Cherry, Bertrand R Huber, Ann C McKee

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

10 authors.

Samantha M CalderazzoDept of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
Morgane L M D ButlerDept of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
Kerry BreenDept of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
Hersh KannerDept of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
Yorghos TripodisDept of Biostatistics, Boston University School of Medicine, Boston, MA, USA.
Thor D SteinDept of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
David M HoltzmanDept. of Neurology, Washington University in St. Louis, St. Louis, MO, USA.
Jonathan D CherryDept of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
Bertrand R HuberDept of Neurology, Boston Medical Center, Boston, MA, USA.
Ann C McKeeDept of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA. amckee@bu.edu.

Funding

Neuropathology CoreP30AG013846 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KOWALL, NEIL W. · 1996 to 2020
$29.1M
Traumatic Brain Injury and Repetitive Head Impacts: Contributions to AD/ADRD and CTE Neuropathology and Resulting Clinical SyndromesU54NS115266 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI STEIN, THOR · 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
Mechanisms of Age-Related TauopathyR01NS095252 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI John Fonda Crary · 2015 to 2026
$3.4M
Epigenetic changes in synaptic and inflammatory genes involved in the age-dependent development of Alzheimer's disease pathologies andcognitive declineRF1AG054156 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, RYU, HOON · 2016 to 2018
$3.4M
Mechanisms of age-related tauopathyRF1NS095252 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI CRARY, JOHN FONDA · 2022 to 2022
$2.5M
Role of T cells in tau-mediated neurodegenerationR01AG085374 · NIA · WASHINGTON UNIVERSITY · PI DAVID M. HOLTZMAN, Jason D Ulrich · 2024 to 2026
$2.2M
Neuroinflammatory Alterations in Post-Traumatic Stress Disorder and Chronic Traumatic EncephalopathyF30NS134280 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI Samantha Calderazzo · 2024 to 2026
$160k
BLRD VA I01 BX002466NIA NIH HHS P30 AG013846NIA NIH HHS R01 AG062348NIA NIH HHS R01AG062348NIA NIH HHS R01 AG085374NIA NIH HHS RF1 AG054156NIA NIH HHS RF1AG054156NIA NIH HHS RF1 AG062348NIH HHS R01AG085374NINDS NIH HHS F30NS134280NINDS NIH HHS R01 NS095252NINDS NIH HHS RF1 NS095252NINDS NIH HHS U01 NS086659NINDS NIH HHS U54 NS115266NINDS NIH HHS U54NS115266U.S. Department of Veterans Affairs I01BX002466U.S. Department of Veterans Affairs I01BX005933
6 · The paper itself

Abstract

Central nervous system (CNS) associated T-cells are present in the meninges and perivascular spaces of healthy brain tissue, but their recruitment into the brain parenchyma is increased by inflammation and hyperphosphorylated tau (p-tau) accumulation. Chronic traumatic encephalopathy (CTE) is a progressive tauopathy associated with exposure to repetitive head impacts (RHI) and definitively diagnosed by the presence of a pathognomonic perivascular p-tau lesion, most commonly at the sulcal depths of the dorsolateral frontal cortex (DLF). Exposure to RHI and CTE is associated with substantial neuroinflammation; however, the involvement of T cells is unknown. Here, we used post-mortem human brain tissue to assess T-cell accumulation in the DLF of 58 individuals exposed to RHI, including 19 with neuropathologically verified Low CTE (stage I-II), 23 with neuropathologically verified High CTE (stage III-IV), and 16 without CTE, as well as 18 controls unexposed to RHI and without CTE. Multiplex immunofluorescence was utilized to label T-cells, microglia, p-tau, and synapses in the leptomeninges, sulcal gray matter, crest gray matter, and white matter. We found that infiltrating T-cells were significantly increased in the sulci across all groups compared to controls, with distinct subtypes in RHI without CTE, compared to Low or High CTE. In addition, T-cell infiltration correlated with the duration of RHI, as measured by years of sports play, and synaptic loss. Meningeal and infiltrating T-cells were elevated in sulci with p-tau depositions and spatially related to MHC2 expressing cells. Meningeal T-cells were also significantly correlated with a younger onset of behavioral symptoms. These data suggest that T-cells may play a role in the chronic inflammation and degeneration associated with RHI and CTE.

Indexed as

Chronic Traumatic EncephalopathyCraniocerebral TraumaMeningesTauopathiestau ProteinsT-LymphocytesAdultAgedAged, 80 and overFemaleHumansMaleMiddle Agedtau ProteinsAdaptive ImmunityCTENeurodegenerationNeuroimmuneNeuroinflammation

Identifiers

PMID41957675
PMCPMC13214261

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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.