Reactive astrocytes promote axonal remodeling and neurological recovery after stroke.

Abstract

Stroke is a leading cause of death and disability in adults worldwide. For decades, the primary approach and goal of therapy for stroke has focused on neuroprotection, namely treating the injured tissue, with interventions designed to reduce the volume of cerebral infarction. Enormous effort in the laboratory has been devoted to the development of neuroprotective agents in an attempt to salvage ischemic neurons in the brain from irreversible injury; however, all these efforts have failed to demonstrate efficacy in clinical trials of stroke. In order to treat stroke, we have to re-conceptualize and redefine our therapeutic targets. Acute neuroprotective treatments for stroke fight a temporal battle of salvaging cerebral tissue before the onset of death, as well as a physiological impediment of delivery of therapy to tissue which has inadequate blood flow. Thus, a more promising therapeutic approach would be to promote remodeling of the central nervous system (CNS) via neurovascular plasticity, and thereby to foster neurological recovery. Stroke affects all cellular elements of the brain i.e., vascular cells, neurons, astrocytes, oligodendrocytes, microglia and ependymocytes. Therefore, to accomplish this and to broaden treatment targets, we must consider therapeutic approaches that benefit multiple cell types, and in our view, particularly, astrocytes, which are in contact with and interact all parenchymal cells (Li et al., 2014).