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Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy.

Overview

Authors: Eda Karakaya1,2,3, Burak Berber1,4,3, Onur Eskiocak5,6,3, Jazlyn Edwards1, Randy Bent Barker1, Sarah Jamil1, Weiguo Li1, Yasir Abdul1, Maria Ericsson7, Thor Stein8,9,10, Ann McKee8,9,10,11, Adviye Ergul1,2, Semir Beyaz5, Onder Albayram1,2,12,13
13 affiliations
  1. Department of Pathology and Laboratory Medicine, ER-AL Neurovascular Protection Laboratory, Medical University of South Carolina, Charleston, SC 29425, USA
  2. Ralph H. Jackson Department of Veterans Affairs Medical Center, Charleston, SC 29425, USA
  3. These authors contributed equally
  4. Department of Biology, Eskisehir Technical University, Eskisehir 26555, Turkey
  5. Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, NY 11724, USA
  6. Graduate Program in Genetics, Stony Brook University, New York, NY 11790, USA
  7. Electron Microscopy Laboratory, Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA
  8. Boston University Alzheimer’s Disease and CTE Center, Boston University School of Medicine, Boston, MA 02118, USA
  9. Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA
  10. VA Boston Healthcare System, Boston, MA 02130, USA
  11. Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA
  12. Department of Neuroscience, Medical University of South Carolina, Charleston, SC 29425, USA
  13. Lead contact
Institutions: Medical University of South Carolina (United States); Ralph H. Johnson VA Medical Center (United States); Eskisehir Technical University (Türkiye); Cold Spring Harbor Laboratory (United States); Stony Brook University (United States); Harvard University (United States); Boston University (United States); VA Boston Healthcare System (United States)
Journal: Cell reports, volume 45, issue 4, article 117135
Dates: published online 25 March 2026; in print March 2026
Type: Research article · Language: English
License: CC BY-NC-ND
Identifiers: DOI 10.1016/j.celrep.2026.117135 · PMID 41887219 · PMCID PMC13276978 · OpenAlex W7140293993
Open access: gold, a free copy (OpenAlex)
Status: code on request (how the code is found and verified)
Categories: other condition (population), stroke (population), traumatic brain injury (population), cellular / molecular (subfield)
Methods: Statistics, Smoothing, state filtering, decompositions, Machine learning, Evoked potentials, Connectivity, Spectral & time-frequency
Keywords: Angiogenesis, Eicosapentaenoic acid, EPA, Traumatic brain injury, Neurovascular Unit, Tbi, Extracellular Matrix Remodeling, Chronic Traumatic Encephalopathy, Cte, Endothelial Metabolism, Precision Nutrition, Cp: Neuroscience, Cp: Metabolism, Context-dependent Vulnerability
Topic: Traumatic Brain Injury and Neurovascular Disturbances (Clinical Neurology, Medicine), according to OpenAlex
Funding: Department of Veterans Affairs (BX000347, IK6 BX004471); NINDS NIH HHS (RF1 NS104573, U54 NS115266, RF1 NS083559, U01 NS086659); Swim Across America (U54NS115266, P30AG072978, U01NS086659); BLRD VA (IK6 BX004471); NIGMS NIH HHS (P20 GM148302); NIA NIH HHS (P30 AG072978); NCI NIH HHS (R37 CA292807); National Institutes of Health (RF1 NS083559, RF1 NS10457, U54DA16511); NIDA NIH HHS (U54 DA016511); The Mark Foundation for Cancer Research (20-028-EDV); Alzheimer's Disease Research Center, University of Pittsburgh; Cold Spring Harbor Laboratory; National Cancer Institute (R37CA292807); G. Harold and Leila Y. Mathers Charitable Foundation
Citations: not cited yet (Europe PMC); 96 references in the paper
Research resources: anti-agrin RRID:AB_11029656, HRP-conjugated secondary antibodies RRID:AB_11125142, anti-matrix metalloproteinase 9 (MMP9) RRID:AB_11157246, anti-phospho-tau (Ser202/Thr205) RRID:AB_223647, RRID:AB_2336404, anti-β-actin-peroxidase conjugate RRID:AB_262011, anti-collagen type IV alpha 1 (Col4a1) RRID:AB_2938081, RRID:AB_3195588, anti-collagen type VI alpha 6 (Col6a6) RRID:AB_3261932, anti-VE-cadherin RRID:AB_3683680, anti-claudin-5 RRID:AB_87321

Abstract

The abstract is not reproduced here: the paper's license (CC BY-NC-ND) does not allow it. Read it in the paper, at the publisher or on Europe PMC.

Code

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Data

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Code and data availability statement

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Read it in the paper: doi.org/10.1016/j.celrep.2026.117135.

Versions

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Version 1, 30 September 2026: the first record

Recorded: type, language, journal, volume, issue, pages, dates, 14 authors, 14 keywords, 14 funders, 95 references, 11 RRIDs.

Cite

This paper

Karakaya, E., Berber, B., Eskiocak, O., Edwards, J., Barker, R. B., Jamil, S., Li, W., Abdul, Y., Ericsson, M., Stein, T., McKee, A., Ergul, A., Beyaz, S., & Albayram, O. (2026). Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy. Cell reports, 45(4), 117135. https://doi.org/10.1016/j.celrep.2026.117135

BibTeX

@article{karakaya2026eicosapentaenoic,
author = {Karakaya, Eda and Berber, Burak and Eskiocak, Onur and Edwards, Jazlyn and Barker, Randy Bent and Jamil, Sarah and Li, Weiguo and Abdul, Yasir and Ericsson, Maria and Stein, Thor and McKee, Ann and Ergul, Adviye and Beyaz, Semir and Albayram, Onder},
title = {{Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy}},
journal = {Cell reports},
year = {2026},
month = mar,
volume = {45},
number = {4},
pages = {117135},
publisher = {Cell Press},
issn = {2211-1247},
doi = {10.1016/j.celrep.2026.117135},
url = {https://doi.org/10.1016/j.celrep.2026.117135},
pmid = {41887219},
pmcid = {PMC13276978}
}

RIS

TY - JOUR
AU - Karakaya, Eda
AU - Berber, Burak
AU - Eskiocak, Onur
AU - Edwards, Jazlyn
AU - Barker, Randy Bent
AU - Jamil, Sarah
AU - Li, Weiguo
AU - Abdul, Yasir
AU - Ericsson, Maria
AU - Stein, Thor
AU - McKee, Ann
AU - Ergul, Adviye
AU - Beyaz, Semir
AU - Albayram, Onder
TI - Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy
T2 - Cell reports
J2 - Cell Rep
PY - 2026
DA - 2026/03/25
VL - 45
IS - 4
SP - 117135
SN - 2211-1247
PB - Cell Press
DO - 10.1016/j.celrep.2026.117135
UR - https://doi.org/10.1016/j.celrep.2026.117135
LA - en
ER -

CSL-JSON

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"language": "en",
"issued": {
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}

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