Serum BD-tau is elevated acutely in CSVD-related recent small subcortical infarct, correlates with infarct size and normalises by 3 months, but was not associated with chronic CSVD neuroimaging features or disease progression, suggesting sensitivity to acute neuronal injury rather than chronic or progressive CSVD.
Key Findings
Results
Baseline serum BD-tau was higher in patients with a recent small subcortical infarct (RSSI) than in controls.
Median 9.54 (7.32-12.20) pg/mL in RSSI patients vs 7.75 (6.18-9.44) pg/mL in controls; P = .003.
Cohort comprised 101 lacunar stroke patients with MRI-confirmed RSSI and 47 controls.
Serum BD-tau was measured using the HD-X SIMOA platform.
Results
Baseline BD-tau correlated with infarct diameter.
Spearman correlation rs = 0.222, P = 0.039.
The correlation was weak-to-modest in magnitude.
Results
BD-tau levels were not related to the time from symptom onset to blood sampling.
rs = 0.150, P = .179.
Results
BD-tau was not associated with chronic CSVD neuroimaging features at any timepoint.
Features examined: white matter hyperintensities, lacunes, microbleeds, and total SVD score.
All P > .05 at baseline, 3 months and 15 months.
Results
BD-tau levels returned to control levels by 3 months and remained stable at 15 months.
At 3 months, difference from controls was not significant (P = .374).
At 15 months, levels remained stable (P = .985).
Blood was sampled at baseline, 3 and 15 months after stroke.
Results
BD-tau was not associated with CSVD progression (new vascular MRI lesions on follow-up) or with functional neurological outcome.
Associations with new vascular lesions on follow-up MRI were not significant.
Associations with functional outcome were also not significant, unlike findings reported in general ischaemic stroke.
Conclusions
The authors interpret BD-tau as reflecting acute neuronal injury rather than chronic or progressive small vessel disease.
BD-tau is elevated acutely in CSVD-related RSSI and normalises by 3 months.
No association with chronic CSVD markers or progression was found.
Prior data linked BD-tau to infarct volume and functional outcome in general ischaemic stroke, but data in lacunar stroke/CSVD were lacking.
What This Means
This study looked at a blood marker called brain-derived tau (BD-tau), which specifically reflects tau protein released from brain tissue, in people who had a small deep brain stroke (lacunar stroke) related to small vessel disease. The researchers measured it in 101 patients shortly after stroke and again at 3 and 15 months, and compared them with 47 controls.
BD-tau was higher in stroke patients than controls soon after the stroke, and it was modestly higher in those with larger infarcts. By 3 months it had fallen to control levels and stayed there. It did not track with the amount of chronic small vessel damage seen on MRI (such as white matter changes, lacunes or microbleeds), with new brain lesions appearing on later scans, or with how well patients functioned later.
This research suggests BD-tau may be a marker of acute brain injury from a small stroke rather than a measure of ongoing or long-term small vessel disease or a predictor of recovery. The effect on infarct size was modest, and the findings come from a single cohort, so further work would be needed to confirm them.
Gattringer T, Haidegger M, Tafrali C, Martinez-Serrat M, Pinter D, Fandler-Höfler S, et al.. (2026). Serum brain-derived tau in lacunar stroke and cerebral small vessel disease.. European stroke journal. https://doi.org/10.1093/esj/aakag133