A1 Refereed original research article in a scientific journal
Blood biomarkers to identify patients with different intracranial lesion combinations after traumatic brain injury
Authors: Koivikko, Pia; Katila, Ari J.; Takala, Riikka SK.; Hossain, Iftakher; Luoto, Teemu M.; Raj, Rahul; Koivisto, Mari; Tenovuo, Olli; Blennow, Kaj; Hutchinson, Peter; Maanpää, Henna-Riikka; Mohammadian, Mehrbod; Newcombe, Virginia F.; Sanchez, Jean-Charles; Tallus, Jussi; van Gils, Mark; Zetterberg, Henrik; Posti, Jussi P.
Publisher: Elsevier BV
Publication year: 2025
Journal: Brain and Spine
Journal name in source: Brain and Spine
Article number: 104195
Volume: 5
eISSN: 2772-5294
DOI: https://doi.org/10.1016/j.bas.2025.104195
Web address : https://doi.org/10.1016/j.bas.2025.104195
Self-archived copy’s web address: https://research.utu.fi/converis/portal/detail/Publication/484689186
Introduction
There is a lack of studies examining the most promising blood biomarkers for traumatic brain injury (TBI) in relation to gross pathology types.
Research question
To examine whether the admission levels of blood biomarkers can discriminate patients with different combinations of traumatic intracranial findings from patients with negative computed tomography (CT) scans.
Material and methods
One hundred thirty patients with all severities of TBI were studied. Seventy-five had CT-positive and 55 CT-negative findings. CT-positive patients were divided into three clusters (CL) using the Helsinki CT score: focal lesions (CL1), mixed lesions (CL2) and mixed lesions + intraventricular haemorrhage (CL3). CT scans were obtained upon admission and blood samples taken within 24 h from admission. S100 calcium-binding protein B (S100B), glial fibrillary acidic protein (GFAP), heart fatty-acid binding protein (H-FABP), neurofilament light (NF-L), interleukin-10 (IL-10), total-tau (t-tau), and β-amyloids 1–40 (Aβ40) and 1–42 (Aβ42) were analysed from plasma samples. CT-negative cluster was used as control.
Results
GFAP, Aβ40 and Aβ42 levels differed between the clusters, but not significantly. NF-L and t-tau discriminated CL1 from CT-negative cluster with AUCs of 0.737 and 0.771, respectively. NF-L, t-tau and GFAP discriminated CL2 from CT-negative cluster with AUCs of 0.839, 0.781 and 0.840, respectively. All biomarkers analysed were able to discriminate CL3 and CT-negative cluster.
Discussion and conclusion
All studied biomarkers distinguished the most severely injured cluster, CL3, from CT-negative cluster. The results may reflect the severity of TBI but also show that biomarkers have a variable ability to identify patients with combinations of intracranial traumatic lesions in the examined time window.
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Funding information in the publication:
PK is supported by State Research Funding (Finland) (#11211) and Maire Taponen Foundation. HZ is a Wallenberg Scholar and a Distinguished Professor at the Swedish Research Council supported by grants from the Swedish Research Council (#2023–00356; #2022–01018 and #2019–02397), the European Union's Horizon Europe research and innovation programme under grant agreement No 101053962, Swedish State Support for Clinical Research (#ALFGBG-71320), the Alzheimer Drug Discovery Foundation (ADDF), USA (#201809–2016862), the AD Strategic Fund and the Alzheimer's Association (#ADSF-21-831376-C, #ADSF-21-831381-C, #ADSF-21-831377-C, and #ADSF-24-1284328-C), the Bluefield Project, Cure Alzheimer's Fund, the Olav Thon Foundation, the Erling-Persson Family Foundation, Familjen Rönströms Stiftelse, Stiftelsen för Gamla Tjänarinnor, Hjärnfonden, Sweden (#FO 2022-0270), the European Union's Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No 860197 (MIRIADE), the European Union Joint Programme – Neurodegenerative Disease Research (JPND 2021-00694), the National Institute for Health and Care Research University College London Hospitals Biomedical Research Centre, and the UK Dementia Research Institute at UCL (UKDRI-1003). PJH is supported by the UK NIHR (Senior Investigator Award, Cambridge BRC, NIHR Global Health Research Group on Acquired Brain and Spine Injury, Brain Injury MedTech Co-operative) and the Royal College of Surgeons of England. IH is supported by the Finnish Medical Foundation, the Paulo Foundation, the Maire Taponen Foundation, the State Research Funding (Finland) and the Orion Research Foundation. VFJN is supported by a National Institute for Health and Care Research (NIHR) Rosetrees Advanced Trust Fellowship. The views expressed in this publication are those of the authors and not necessarily those of the National Health Service, the National Institute for Health Research, Rosetrees Trust or the Department of Health and Social Care. KB is supported by the Swedish Research Council (#2017–00915 and #2022–00732), the Swedish Alzheimer Foundation (#AF-930351, #AF-939721 and #AF-968270), Hjärnfonden, Sweden (#FO 2017-0243 and #ALZ 2022-0006), the Swedish state under the agreement between the Swedish government and the County Councils, the ALF-agreement (#ALFGBG-715986 and #ALFGBG-965240), the European Union Joint Program for Neurodegenerative Disorders (JPND 2019-466-236), the Alzheimer's Association 2021 Zenith Award (ZEN-21-848495), and the Alzheimer's Association 2022–2025 Grant (SG-23-1038904 QC). JPP is supported by the Research Council of Finland (Grant #60063), Maire Taponen Foundation, and State Research Funding (Finland) (#11129).
