Neuroinflammation is Associated with Brain Extracellular TAU-Protein Release after Spontaneous Subarachnoid Hemorrhage.

Schiefecker, Alois Josef; Dietmann, Anelia; Beer, Ronny; Pfausler, Bettina; Lackner, Peter; Kofler, Mario; Fischer, Marlene; Broessner, Gregor; Sohm, Florian; Mulino, Miriam; Thomé, Claudius; Humpel, Christian; Schmutzhard, Erich; Helbok, Raimund (2017). Neuroinflammation is Associated with Brain Extracellular TAU-Protein Release after Spontaneous Subarachnoid Hemorrhage. Current drug targets, 18(12), pp. 1408-1416. Bentham Science Publishers

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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 high-grade (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). CONCLUSIONS 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.

Item Type:

Journal Article (Original Article)


04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurology

UniBE Contributor:

Dietmann, Anelia


600 Technology > 610 Medicine & health




Bentham Science Publishers




Stefanie Hetzenecker

Date Deposited:

20 Mar 2017 15:20

Last Modified:

28 Oct 2017 01:30

PubMed ID:



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