title: Neuronal restoration following ischemic stroke: influences, barriers, and therapeutic potential.
abstract: Neurogenesis, the birth of new neurons, occurs throughout life in the subventricular zone and produces immature neurons that migrate tangentially through the rostral migratory stream to the olfactory bulb. This migration is tightly regulated by both structural and chemical influences. Interestingly, brain insults such as ischemic stroke increase neurogenesis and redirect neuroblast migration to the injury site. This injury-redirected neurogenesis and migration is coupled with angiogenic vasculature and is influenced by many of the factors that positively and negatively affect migration under developmental or normal adult conditions. Additionally, cytokines and chemokines such as stromal cell-derived factor-1 strongly influence neuronal migration poststroke. However, neuronal repopulation or brain regeneration is extremely limited. This limitation may potentially be due to the hostile poststroke microenvironment including the formation of the physical and chemical barriers of glial scar. Furthermore, interspecies differences in poststroke neurogenesis between rodents and humans complicate the translation of experimental results to humans. Despite these challenges, many drugs and other potential therapies have recently been evaluated for potential neurogenic properties poststroke. Improved understanding of poststroke neurorepair may lead to new and more effective neurorestorative therapies.
authors: Texas A&M College of Medicine, Bryan, TX, USA.
authors: Michael P
authors: MP
authors: Kahle
authors: Gregory J
authors: GJ
authors: Bix
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000150:complications; D002454:Cell Differentiation; D002465:Cell Movement; D006801:Humans; D055495:Neurogenesis; D009474:Neurons / Q000502:physiology*; D012038:Regeneration / Q000502:physiology*; D020521:Stroke / Q000209:etiology / Q000473:pathology*
keywords: SDF-1; glial scar; neurogenesis; perlecan domain V; regeneration; stroke