Title:Neuroinflammation is Associated with Brain Extracellular TAU-Protein Release After Spontaneous Subarachnoid Hemorrhage
Volume: 18
Issue: 12
Author(s): Alois Josef Schiefecker*, Anelia Dietmann, Ronny Beer, Bettina Pfausler, Peter Lackner, Mario Kofler, Marlene Fischer, Gregor Broessner, Florian Sohm, Miriam Mulino, Claudius Thomé, Christian Humpel, Erich Schmutzhard and Raimund Helbok
Affiliation:
- Department of Neurology, Medical University of Innsbruck, Anichstrasse 35, A-6020 Innsbruck,Austria
Keywords:
Neuroinflammation, tau protein, intracerebral hemorrhage, interleukin-6, cerebral microdialysis.
Abstract: Introduction: Animal data suggest an association between neuroinflammation and secondary
brain injury including axonal injury after aneurysmal subarachnoid hemorrhage (aSAH). We
sought to study the association between brain extracellular interleukin (IL)-6 and TAU-protein levels
as a surrogate marker for neuroinflammation and axonal injury in patients with poor grade aSAH.
Methods: Prospectively collected data from 26 consecutive poor-grade aSAH patients with multimodal
neuromonitoring including cerebral microdialysis (CMD) were retrospectively analyzed. IL-6
and TAU-protein levels were analyzed using ELISA from a single CMD-sample every 24 hours and
correlated with brain metabolic and hemodynamic parameters. Patients were dichotomized to highgrade
(N=10) or low-grade (N=16) neuroinflammation according to their median CMD-IL-6 levels.
Data were analyzed using generalized estimating equations to account for multiple within-subject
measurements.
Results: Perilesional probe location (P=0.02) and aSAH related intracerebral hemorrhage (aICH) volume
(P=0.003) at admission were associated with high-grade neuroinflammation. Brain extracellular
TAU-protein levels (P=0.001), metabolic distress and delayed cerebral infarction (DCI; P=0.001)
were linked to high-grade neuroinflammation. Relative or absolute phosphor-TAU levels were not
correlated with CMD-IL-6 levels. High-grade neuroinflammation was a predictor for worse outcome
three months after ictus, independently from probe location, initial Hunt&Hess grade and age
(P=0.01).
Conclusion: Neuroinflammation after aSAH is associated with intraparenchymal bleeding, deranged
cerebral metabolism and TAU-protein release. The impact of potential anti-inflammatory treatment
strategies on secondary brain injury after aSAH has to be investigated in future studies.
