Improving neurorepair in stroke brain through endogenous neurogenesis-enhancing drugs

Abstract

Stroke induces not only cell death but also neurorepair. De novo neurogenesis has been found in the subventricular zone of the adult mammalian brain days after stroke. Most of these newly generated cells die shortly after the insult. Recent studies have shown that pharmacological manipulation can improve the survival of endogenous neuroprogenitor cells and neural regeneration in stroke rats. As these drugs target the endogenous reparative processes that occur days after stroke, they may provide a prolonged window for stroke therapy. Here, we discuss endogenous neurogenesis-enhancing drugs and review the general status of stroke therapeutics in evaluating the field of pharmacotherapy for stroke.

Sodium/Hydrogen Exchanger 1 Participates in Early Brain Injury after Subarachnoid Hemorrhage both in vivo and in vitro via Promoting Neuronal Apoptosis

“…Aneurysm rupture is the major cause of SAH (nearly 85% of cases of spontaneous SAH), and approximately 12% patients die before receiving medical attention, 33% within 48 h and 50% within 30 days after initial hemorrhage 3 –5 . Despite the improvements achieved in the treatment and management of SAH patients, the prognosis is still not satisfactory 6 –11 . Historically, many research studies have focused mainly on therapy targeted cerebral vasospasm (CVS) after SAH, but the clinical outcomes are unsatisfactory, and they fail to decrease the incidence of delayed cerebral ischemia and mortality 3,12 –14 .…”

Detection of Crossed Cerebellar Diaschisis by Intravoxel Incoherent Motion MR Imaging in Subacute Ischemic Stroke

“…When an ischemic cerebral stroke occurs, a series of excitotoxicity, apoptosis, and cell death is activated, which may lead to morbidity and mortality 1 . As a common radiological phenomenon, crossed cerebellar diaschisis (CCD) is characterized by hypoperfusion and hypometabolism of the contralateral cerebellar hemisphere, which results from the dysfunction of the related supratentorial region 2 .…”