tissue or organ can, when applied close to the threshold of damage, activate endogenous protective mechanisms thus potentially lessening the impact of subsequent, more severe stimuli in the brain tissue. The phenomenon of ischemic tolerance is explained with the help of different experimental models constituting the main pharmacological targets to induce preventive neuroprotection. Deep insights are given into the main molecular mechanisms for inducing ischemic tolerance. Several pharmacological agents and therapeutic strategies are described that have been demonstrated experimentally to induce an ischemic tolerance related to their pleiotropic preconditioning properties. The present book will open a window into the understanding of endogenous neuroprotection and, potentially, the opportunity to utilise these mechanisms in the clinic to treat patients with stroke and other CNS disorders.

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