Stroke Recovery

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LITERATURE REVIEW

Stroke is one of the major health problems worldwide and a leading cause of disability. But the treatment options for the management of stroke are limited. Thrombolytic reperfusion with recombinant tissue plasminogen activator (t-PA) is employed in acute phase in only less than 3% of all ischemic stroke patients while standard treatments involving rehabilitation provide some benefits for the recovery during chronic phase. However, many high-profile failures in a wide spectrum of pharmacologic neuroprotection trials have led to some pessimism in the field.[1] Recent findings suggest that enhancement of angiogenesis after focal cerebral ischemia may provide novel opportunities for better outcomes during stroke recovery.[2] Nowadays it is appreciated that new treatment strategies should target cerebral blood vessels and induction of angiogenesis will stimulate recovery processes including neurogenesis, synaptogenesis, and neuronal and synaptic
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Some of the major factors are vascular endothelial growth factor (VEGF), Fibroblast growth factor-2 (FGF-2/bFGF), Platelet-Derived growth factor-Beta (PDGF-beta), Transforming growth factor-beta (TGF-beta). These angiogenic peptides are found to be upregulated following ischemic insults to promote micro vessel formation and brain remodeling.[1] Among these numerous endogenous angiogenic regulators, VEGF is the prototypical and most studied proangiogenic mediator in stroke.[2, 3] VEGF is an endothelial cell-specific mitogen which also plays a role in the regulation of vascular permeability. VEGF executes its biological effect through two tyrosine kinase receptors, Flt-1 (VEGFr-1) and KDR (VEGFR-2).[15] It has been known to be the potent mediator of neurorestoration following stroke by promoting neurogenesis and

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