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Intravenous brain-derived neurotrophic factor enhances poststroke sensorimotor recovery and stimulates neurogenesis.

Artikel i vetenskaplig tidskrift
Författare Wolf-Rüdiger Schäbitz
Tobias Steigleder
Christiana M Cooper-Kuhn
Stefan Schwab
Clemens Sommer
Armin Schneider
Hans-Georg Kuhn
Publicerad i Stroke; a journal of cerebral circulation
Volym 38
Nummer/häfte 7
Sidor 2165-72
ISSN 1524-4628
Publiceringsår 2007
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 2165-72
Språk en
Länkar dx.doi.org/10.1161/STROKEAHA.106.47...
Ämnesord Animals, Behavior, Animal, physiology, Brain, anatomy & histology, drug effects, pathology, physiology, Brain Ischemia, drug therapy, pathology, rehabilitation, Brain-Derived Neurotrophic Factor, administration & dosage, pharmacology, therapeutic use, Cell Differentiation, drug effects, Cell Movement, drug effects, Male, Neurons, drug effects, physiology, Random Allocation, Rats, Rats, Wistar, Recovery of Function, Stem Cells, drug effects, Stroke, drug therapy, pathology, rehabilitation, Treatment Outcome
Ämneskategorier Neurovetenskap

Sammanfattning

BACKGROUND AND PURPOSE: The discovery of spontaneous neuronal replacement in the adult brain has shifted experimental stroke therapies toward a combined approach of preventing neuronal cell death and inducing neuronal plasticity. Brain-derived neurotrophic factor (BDNF) was shown to induce antiapoptotic mechanisms after stroke and to reduce infarct size and secondary neuronal cell death. Moreover, in intact animals, BDNF is a potent stimulator of adult neurogenesis. METHODS: The current study analyzed the effects of BDNF on induction of neuronal progenitor cell migration and sensorimotor recovery after cortical photothrombotic stroke. RESULTS: Daily intravenous bolus applications of BDNF during the first 5 days after stroke resulted in significantly improved sensorimotor scores up to 6 weeks. At the structural level, BDNF significantly increased neurogenesis in the dentate gyrus and enhanced migration of subventricular zone progenitor cells to the nearby striatum of the ischemic hemisphere. BDNF treatment could not, however, further stimulate progenitor cell recruitment to the cortex. CONCLUSIONS: These findings consolidate the role of BDNF as a modulator of neurogenesis in the brain and as an enhancer of long-term functional neurological outcome after cerebral ischemia.

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