Microglia and macrophages play critical roles in brain repair following injury, with their polarization into distinct phenotypes influencing recovery. Traditionally, the adult brain was viewed as static, but recent research shows it has regenerative capacity. Microglia/macrophages clear debris and support repair, but excessive activation can hinder recovery. These cells can adopt M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes, with M2 promoting neurogenesis, axonal regeneration, and remyelination. However, M1 activation can be detrimental. The balance between these phenotypes is crucial for effective repair. Recent studies highlight the complexity of microglia/macrophage polarization, with multiple subtypes (e.g., M2a, M2b, M2c) and environmental cues influencing their behavior. Factors such as injury location, time, and aging affect polarization dynamics. Microglia differ from peripheral macrophages in function and response to injury. Therapeutic strategies should focus on modulating the balance between M1 and M2 phenotypes rather than complete suppression. Emerging research on regulatory molecules, extracellular signals, and intracellular pathways offers new targets for intervention. Therapeutic approaches include cell transplantation, targeting protective factors, and using molecular switches to influence polarization. Challenges remain in translating findings to clinical settings, with ongoing research needed to understand the precise roles of microglia/macrophages in CNS repair.Microglia and macrophages play critical roles in brain repair following injury, with their polarization into distinct phenotypes influencing recovery. Traditionally, the adult brain was viewed as static, but recent research shows it has regenerative capacity. Microglia/macrophages clear debris and support repair, but excessive activation can hinder recovery. These cells can adopt M1 (pro-inflammatory) or M2 (anti-inflammatory) phenotypes, with M2 promoting neurogenesis, axonal regeneration, and remyelination. However, M1 activation can be detrimental. The balance between these phenotypes is crucial for effective repair. Recent studies highlight the complexity of microglia/macrophage polarization, with multiple subtypes (e.g., M2a, M2b, M2c) and environmental cues influencing their behavior. Factors such as injury location, time, and aging affect polarization dynamics. Microglia differ from peripheral macrophages in function and response to injury. Therapeutic strategies should focus on modulating the balance between M1 and M2 phenotypes rather than complete suppression. Emerging research on regulatory molecules, extracellular signals, and intracellular pathways offers new targets for intervention. Therapeutic approaches include cell transplantation, targeting protective factors, and using molecular switches to influence polarization. Challenges remain in translating findings to clinical settings, with ongoing research needed to understand the precise roles of microglia/macrophages in CNS repair.