<unk>  is the use of the glycoprotein<unk>  (Epo) for<unk> . Epo controls erythropoiesis, or red blood cell production.<unk>  and its receptor were thought to be present in the central nervous system according to experiments with antibodies that were subsequently shown to be nonspecific. While epoetin alpha is capable of crossing the blood brain barrier via active transport the amounts appearing in the CNS are very low. The possibility that Epo might have effects on neural tissues resulted in experiments to explore whether Epo might be tissue protective. The reported presence of Epo within the spinal fluid of infants and the expression of Epo-R in the spinal cord, suggested a potential role by Epo within the CNS therefore Epo represented a potential therapy to protect photoreceptors damaged from hypoxic pretreatment. In some animal studies<unk>  has been shown to protect nerve cells from hypoxia-induced glutamate toxicity. Epo has also been reported to enhance nerve recovery after spinal trauma. Celik and associates investigated motor neuron apoptosis in rabbits with a transient global spinal ischemia model. The functional neurological status of animals given RhEpo was better after recovery from anesthesia, and kept improving over a two-day period. The animals given saline demonstrated a poor functional neurological status and showed no significant improvements. These results suggested that RhEpo has both an acute and delayed beneficial action in ischemic spinal cord injury. In contrast to these results, numerous studies suggested that Epo had no neuroprotective benefit in animal models and EpoR was not detected in brain tissues using anti-EpoR antibodies that were shown to be sensitive and specific.
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