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Despite increasing knowledge of the biochemical mechanisms that occur in the brain following an ischemic insult and the availability of several diverse animal models of stroke, there are still no drugs that can be given to stroke patients soon after the onset of symptoms to minimize the subsequent neurological damage. To date, the thrombolytic compound recombinant tissue Plasminogen Activator (rt-PA) remains the only approved drug for the treatment of stroke. At present, intravenous administration of rt-PA is the only proven effective treatment to re-establish cerebral blood flow in the case of acute vessel occlusion, but unfortunately, only few patients with acute ischemic stroke are qualified to receive this drug. The failure of rt-PA to achieve rapid reperfusion in many patients and its bleeding risk have prompted the development of fibrinolytic agents with greater fibrin specificity and better risk-benefit profiles, such as tenecteplase or desmoteplase, which are now under active investigation. Early restoration of blood flow remains the treatment of choice for limiting brain injury following stroke, but a second fundamental goal of intervention is to protect neurons by interrupting or slowing the ischemic cascade. Current research is being done to develop neuroprotective agents that are able to block amino acid pathways and decrease neurotransmitter activity of injured tissue. Drugs blocking voltage-dependent calcium channels were effective in stroke rodent models but the results of clinical trials have been often discouraging. Overactivation of the N-methyl-D-aspartate receptor (NMDAR) is crucial for neuronal death after stroke. Several compounds that interfere with glutamate receptor activation have been developed and tested, in particular noncompetitive NMDA antagonists. However, their clinical use is limited by intolerable side effects, including some psycomimetic symptoms, as these blockers may also impair some key brain functions mediated by the same receptor. Accumulating evidence strongly suggests that apoptosis contributes to neuronal cell death in stroke injury and currently several caspase inhibitors are under investigation, but to date the efficacy of antiapoptotic agents in human stroke patients has not yet been tested. Anti-inflammatory approaches to stroke treatment intended

PPAR Agonism as New Pharmacological Approach to the Management of Acute Ischemic Stroke