Neuroprotection therapies have made limited progress in recent years. Several compounds shown to be efficacious in animals were tested in humans in cost-expensive trials. Unfortunately none of these studies were able to demonstrate efficacy under clinical conditions in patients. In order to establish treatments that are of benefit not only in animals but also humans, new strategies are clearly needed, comprising (i) new factors mimicking intrinsic mechanisms that the brain itself makes use of, (ii) novel delivery techniques allowing drugs to pass the blood-brain barrier more efficaciously than before, (iii) better, functionally relevant readouts of brain recovery and (iv) strategies that are of usefulness not only in the acute, but also post-acute stroke phase. According to these strategies, EPO's neuroprotective and restorative effects on ischemic brain injury will be reviewed.

References: 

1. Kilic et al., 2005a. Brain-derived erythropoietin protects from focal cerebral ischemia by dual activation of ERK-1/-2 and Akt pathways. FASEB J. 2005, 19: 2026–8.

2. Kilic et al., 2005b. Erythropoietin protects from axotomy-induced degeneration of retinal ganglion cells by activating ERK-1/-2. FASEB J. 2005, 19: 249–51.

3. Reitmeir, R., Kilic, E., Kilic, U., Bacigaluppi, M., ElAli A, Salani, G., Pluchino, S., Gassmann, M., Hermann, DM. Post-acute delivery of erythropoietin induces stroke recovery by promoting perilesional tissue remodeling and contralesional pyramidal tract plasticity. Brain. 2011, 134:84–99.