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Brain Protein Improves Stroke Symptoms In Rats, Even When Injected After 3 Days

A protein naturally occurring in the brain improves recovery from stroke when injected up to three days after the onset of the stroke, and could be used as an effective stroke drug. A study in rats published in the open access journal BMC Biology shows that an injection of Granulocyte-Colony Stimulating Factor (G-CSF), whose function in the brain is to control the formation of neurons and counteract neurone death, reduces the size of the area affected by a stroke by a third when injected four hours after the onset of the stroke.

A protein naturally occurring in the brain improves recovery from stroke when injected up to three days after the onset of the stroke, and could be used as an effective stroke drug. A study in rats published in the open access journal BMC Biology shows that an injection of Granulocyte-Colony Stimulating Factor (G-CSF), whose function in the brain is to control the formation of neurons and counteract neurone death, reduces the size of the area affected by a stroke by a third when injected four hours after the onset of the stroke. The study also shows that regular, delayed injections of G-CSF, starting up to three days after experimental stroke, are effective in restoring motor functions in rats.

G-CSF is known to improve recovery after a stroke, and it is currently being tested for use in humans. The BMC Biology study is the first to show that G-CSF can be effective when injected this late after a stroke event.

Armin Schneider from Sygnis Bioscience AG (formerly known as Axaron Bioscience AG) in Heidelberg, Germany, and Wolf-Rüdiger Schäbitz from the Neurology department in Münster, Germany, together with colleagues from the universities of Heidelberg and Erlangen, used rat models of two different types of stroke to assess the effect of an injection of G-CSF on recovery.

The first model was used to assess the impact of G-CSF on the size of the brain area affected by the stroke, which is identified by the presence of dead neurons. In this model, the animals were injected with a single dose of G-CSF at 60µg/kg body weight four hours after the stroke. The researchers demonstrate that the size of the affected area is reduced by 34.5% in the rats that received G-CSF four hours after the stroke.

The second model was used to assess the effect of G-CSF on the functional performance of the animals. In this model, the rats were injected 10 µg/kg body weight of G-CSF, starting 24 or 72 hours after the stroke, for a period of ten days. Rats treated with G-CSF for ten days after the stroke performed significantly better in an exercise designed to test their physical abilities and coordination than rats that had been treated with placebo.

The results of the current study should help to guide the design of future studies in humans.

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