Skip to content
DraconiticResearch
Search Sources API
201,818 studies31 sourcesUpdated 6 min ago
Peer-reviewedCC BY-NCEuropean stroke journal

Serum brain-derived tau in lacunar stroke and cerebral small vessel disease.

3 more authors
4 affiliations
  1. 1Department of Neurology, Medical University of Graz, Graz, Austria.
  2. 2Department of Neurology, University Hospital Wiener Neustadt - Hochegg, Wiener Neustadt, Austria.
  3. 3Department of Medicine, Danube Private University, Krems, Austria.
  4. 4Division of Neuroradiology, Vascular and Interventional Radiology, Department of Radiology, Medical University of Graz, Graz, Austria.

Abstract

Introduction

Brain-derived tau (BD-tau) selectively quantifies tau of central nervous system origin in blood and has demonstrated strong correlations with infarct volume and functional outcome in general ischaemic stroke, but data in lacunar stroke and cerebral small vessel disease (CSVD) are lacking.Patients and methods

In a prospectively collected cohort of 101 lacunar stroke patients with an MRI-confirmed recent small subcortical infarct (RSSI) and 47 controls, we measured serum BD-tau using the HD-X SIMOA platform at baseline and 3 and 15 months after stroke. We examined associations of BD-tau with infarct size, chronic CSVD neuroimaging features (white matter hyperintensities [WMHs], lacunes, microbleeds, total SVD score), CSVD progression on follow-up MRI and functional outcome.Results

Baseline serum BD-tau was higher in RSSI patients than controls (median 9.54 [7.32-12.20] vs 7.75 [6.18-9.44] pg/mL; P = .003) and correlated with infarct diameter (rs = 0.222, P = 0.039). Brain-derived tau did not correlate with time from stroke symptom onset to blood sampling (rs = 0.150, P = .179). Brain-derived tau was not associated with chronic CSVD neuroimaging features (WMHs, lacunes, microbleeds, SVD score; all P > .05) at any timepoint. Longitudinally, BD-tau returned to control levels by 3 months (P = .374) and remained stable at 15 months (P = .985). Brain-derived tau was neither associated with new vascular MRI lesions on follow-up nor functional neurological outcome.Conclusion

Serum BD-tau is elevated acutely in CSVD-related RSSI, correlates with infarct size and normalises by 3 months. Brain-derived tau was not associated with chronic CSVD neuroimaging features or disease progression, suggesting sensitivity to acute neuronal injury rather than chronic or progressive CSVD.

Related

  1. Risk factors for acute ischemic stroke of small vessel occlusion in elderly patients with cerebral small vessel disease and establishment of a prediction model
    Xiao Li, Ling Fang, Libo Lu +2
    BMC Cardiovascular DisordersPeer-reviewedCC BY-NC-ND 4.0Full textNeurologyPMC
  2. Warfarin anticoagulation control and risks of cerebral small vessel disease and cognitive impairment among elderly patients with ischemic stroke and atrial fibrillation: a retrospective cohort study
    Dan Zhao, Wenping He, Zhifei Shen +2
    Frontiers in NeurosciencePeer-reviewedCC BY 4.0Full textCardiovascular medicineCrossref
  3. Effects of pentoxifylline on cognitive deficits in cerebral small vessel disease: a prospective, randomized controlled, multi-center trial protocol
    Ying Chen, Wan Jiang, Xin Zhang +2
    TrialsPeer-reviewedCC BY 4.0Clinical trials & evidence synthesisCrossref
  4. Chronic Atrial and Intestinal Dysrhythmia Syndrome: A Distinct Monogenic Cause of Cerebral Small Vessel Disease
    C. Dallaire-Theroux, A. Nehme, F. Brunet +8
    medRxivPreprintAll rights reservedFull textNeurologymedRxiv
  5. Association of Glymphatic Imaging Markers With Clinical Outcomes and Cerebral Small Vessel Disease Burden After Intracerebral Hemorrhage
    Xiao Hu, Zuoqiao Li, Zijie Wang +7
    Brain and behaviorPeer-reviewedCC BYFull textGeneral medicineEurope PMC
BibTeX
@article{gattringer2026serum,
  title = {{Serum brain-derived tau in lacunar stroke and cerebral small vessel disease.}},
  author = {Thomas Gattringer and Melanie Haidegger and Cansu Tafrali and Maria Martinez-Serrat and Daniela Pinter and Simon Fandler-Höfler and Markus Kneihsl and Stephan Seiler and Sebastian Eppinger and Christian Kiss and Roberta Bichler and Michaela T Haindl and Stefan Ropele and Christian Enzinger and Michael Khalil},
  journal = {European stroke journal},
  year = {2026},
  month = nov,
  doi = {10.1093/esj/aakag133},
  url = {https://europepmc.org/article/MED/42969846},
  note = {CC BY-NC},
}
RIS
TY  - JOUR
TI  - Serum brain-derived tau in lacunar stroke and cerebral small vessel disease.
AU  - Thomas Gattringer
AU  - Melanie Haidegger
AU  - Cansu Tafrali
AU  - Maria Martinez-Serrat
AU  - Daniela Pinter
AU  - Simon Fandler-Höfler
AU  - Markus Kneihsl
AU  - Stephan Seiler
AU  - Sebastian Eppinger
AU  - Christian Kiss
AU  - Roberta Bichler
AU  - Michaela T Haindl
AU  - Stefan Ropele
AU  - Christian Enzinger
AU  - Michael Khalil
PY  - 2026
DA  - 2026/11/01
JO  - European stroke journal
DO  - 10.1093/esj/aakag133
UR  - https://europepmc.org/article/MED/42969846
AB  - Introduction  Brain-derived tau (BD-tau) selectively quantifies tau of central nervous system origin in blood and has demonstrated strong correlations with infarct volume and functional outcome in general ischaemic stroke, but data in lacunar stroke and cerebral small vessel disease (CSVD) are lacking.Patients and methods  In a prospectively collected cohort of 101 lacunar stroke patients with an MRI-confirmed recent small subcortical infarct (RSSI) and 47 controls, we measured serum BD-tau using the HD-X SIMOA platform at baseline and 3 and 15 months after stroke. We examined associations of BD-tau with infarct size, chronic CSVD neuroimaging features (white matter hyperintensities [WMHs], lacunes, microbleeds, total SVD score), CSVD progression on follow-up MRI and functional outcome.Results  Baseline serum BD-tau was higher in RSSI patients than controls (median 9.54 [7.32-12.20] vs 7.75 [6.18-9.44] pg/mL; P = .003) and correlated with infarct diameter (rs = 0.222, P = 0.039). Brain-derived tau did not correlate with time from stroke symptom onset to blood sampling (rs = 0.150, P = .179). Brain-derived tau was not associated with chronic CSVD neuroimaging features (WMHs, lacunes, microbleeds, SVD score; all P > .05) at any timepoint. Longitudinally, BD-tau returned to control levels by 3 months (P = .374) and remained stable at 15 months (P = .985). Brain-derived tau was neither associated with new vascular MRI lesions on follow-up nor functional neurological outcome.Conclusion  Serum BD-tau is elevated acutely in CSVD-related RSSI, correlates with infarct size and normalises by 3 months. Brain-derived tau was not associated with chronic CSVD neuroimaging features or disease progression, suggesting sensitivity to acute neuronal injury rather than chronic or progressive CSVD.
SN  - 2396-9873
SN  - 2396-9881
ER  -