• Andreas Bitsch, Claudia Horn, Yvonne Kemmling, Maria Seipelt, Uwe Hellenbrand, Michael Stiefel, Barbara Ciesielczyk, Lukas Cepek, Erik Bahn, Peter Ratzka, Hilmar Prange, and Markus Otto.
• Department of Neurology, Ruppiner Kliniken GmbH, Neuruppin, Germany. abitsch@t-online.de
• Eur. Neurol. 2002 Jan 1; 47 (1): 45-51.

AbstractBiochemical markers of brain damage, e.g. ischemic stroke, should reflect the volume of irreversibly damaged brain parenchyma and the clinical outcome in a single patient in order to allow estimation of prognosis at an early stage. Tau protein, which derives predominantly from neurons and axons, is elevated in the cerebrospinal fluid of patients with neurodegenerative disease. This makes tau protein a potential marker of neuronal/axonal injury. In order to test this hypothesis, the current study aimed at showing that tau protein is measurable in the blood after acute ischemic stroke and that it correlates with clinical disability and stroke volume. In a longitudinal prospective study we measured tau protein serum levels with an ELISA in 30 patients longitudinally after ischemic stroke. Tau protein was detectable within 5 days after ischemia in the sera of 7/20 patients with MRI-proven infarction and in 2/10 patients with transitory ischemic attack; both of them had a small infarction visible on the MRI scan. Tau protein was measurable within 6 h after symptom onset, peaked after 3-5 days and correlated with infarct volume and disability after 3 months. In conclusion, serum tau protein is a candidate marker of axonal injury. In stroke, its clinical use is limited, because it is detectable only in a proportion of patients.Copyright 2002 S. Karger AG, Basel

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