Brain derived proteins as markers of acute stroke: their relation to pathophysiology, outcome prediction and neuroprotective drug monitoring.

PURPOSE: Ischemic stroke is associated with a variety pathophysiological changes affecting both glial and neuronal brain tissue. These changes are mirrored in the release of specific proteins into peripheral blood. Neurone-specific enolase (NSE), protein S100B and glial fibrillary acidic protein (GFAP) are those proteins investigated most often as peripheral surrogate markers of brain damage after stroke in humans. METHODS AND
RESULTS: In the present article we present data which show that the release patterns of neuronal and glial tissue derived proteins after acute stroke are associated with the neuroradiological and neurobehavioral consequences of ischemic brain lesions and, additionally, may be useful in short-term outcome prediction. Kinetics of protein serum concentrations, however, are highly dependent on subtype of stroke lesions and do not merely reflect the degree of brain damage. They rather express complex neuronal-glial interactions as a (patho-)physiological consequence of ischemic brain lesions. We further demonstrate that S100B release patterns do reflect successful neuroprotective drug treatment with recombinant human erythropoietin (EPO) in acute stroke patients.
CONCLUSIONS: The analysis of poststroke serum concentrations of glial tissue derived proteins might be a promising strategy to monitor and evaluate neuroprotective approaches in stroke treatment.