Neuroinflammation strokes the brain: A double-edged sword in ischemic stroke.

Abstract

Stroke is a major cause of death and disability worldwide. It is characterized by a highly interconnected and multiphasic neuropathological cascade of events, in which an intense and protracted inflammatory response plays a crucial role in worsening brain injury. Neuroinflammation, a key player in the pathophysiology of stroke, has a dual role. In the acute phase of stroke, neuroinflammation exacerbates brain injury, contributing to neuronal damage and blood-brain barrier disruption. This aspect of neuroinflammation is associated with poor neurological outcomes. Conversely, in the recovery phase following stroke, neuroinflammation facilitates brain repair processes, including neurogenesis, angiogenesis, and synaptic plasticity. The transition of neuroinflammation from a harmful to a reparative role is not well understood. Therefore, this review seeks to explore the mechanisms underlying this transition, with the goal of informing the development of therapeutic interventions that are both time- and context-specific. This review aims to elucidate the complex and dual role of neuroinflammation in stroke, highlighting the main actors, biomarkers of the disease, and potential therapeutic approaches.