Neuroprotection can be defined as the protection of cell bodies and neuronal and glial processes by strategies that impede the development of irreversible ischemic injury by effects on the cellular processes involved. Neuroprotection can be achieved using pharmaceutical or physiological therapies that directly inhibit the biochemical, metabolic, and cellular consequences of ischemic injury, or by using indirect approaches such as t-PA and mechanical devices to restore tissue perfusion. The complex and overlapping pathways involving excitotoxicity, ionic imbalance, oxidative and nitrative stress, and apoptotic-like mechanisms have been reviewed above. Each of these pathways offers several potential therapeutic targets, several of which have proved successful in reducing ischemic injury in animal models. However, the successful translation of experimental results into clinical practice remains elusive.

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