
Potential of Brain-Derived Tau to Monitor Acute Brain Injury in Stroke: Steffen Tiedt, MD, PhD
The neurologist at LMU Munich University Hospital discussed newly published data supporting plasma brain-derived tau as a dynamic biomarker of infarct growth and treatment response in acute ischemic stroke. [WATCH TIME: 4 minutes]
WATCH TIME: 4 minutes
“Stroke gives us a uniquely defined onset and clear imaging correlates, which makes it an ideal condition to study acute brain injury. What we observed is that brain-derived tau rises in parallel with tissue damage and even reflects treatment success, which is exactly what we would hope for in a biomarker.”
Despite advances in imaging and reperfusion therapies, acute ischemic stroke lacks a blood-based biomarker capable of dynamically tracking brain injury. Clinicians routinely measure laboratory markers to assess injury in organs such as the heart or liver, yet no equivalent tool exists for real-time monitoring of cerebral tissue damage. The ability to quantify ongoing neuronal injury through a simple blood test could improve prognostication, guide treatment decisions, and potentially serve as a surrogate end point in clinical trials.
In a recently published prospective study, Steffen Tiedt, MD, PhD, and colleagues evaluated plasma brain-derived tau (BD-tau) in 502 patients with acute ischemic stroke, with serial sampling from admission through day 7. Using a single-molecule detection assay designed to selectively quantify tau originating from the central nervous system, the team demonstrated that higher admission BD-tau levels correlated with more extensive early injury on computed tomography and predicted larger final infarct volumes.
Rising BD-tau levels between admission and day 2 were associated with infarct growth, and concentrations continued to increase through day 7. In an independent multicenter cohort (n = 519) also evaluated in the analysis, BD-tau outperformed imaging-derived infarct volume in predicting functional outcomes up to 36 months. Similarly, in another biomarker substudy of a phase 3 trial evaluating nerinetide (n = 193), BD-tau increases were 49% smaller in the treatment group versus placebo, suggesting potential utility in detecting treatment effects.
Following publication, Tiedt, a neurologist at LMU University Hospital Munich and investigator at the Institute for Stroke and Dementia Research, spoke with NeurologyLive® about the development of BD-tau and its clinical implications. In the discussion, he explained how distinguishing central nervous system–derived tau from peripheral isoforms enhanced specificity, how BD-tau tracks infarct evolution and secondary events, and why this biomarker may represent a long-awaited tool for monitoring acute brain injury in stroke.

















