Neurogenesis After Stroke: A Therapeutic Perspective

Abstract

Stroke is a major cause of death and disability worldwide. Yet therapeutic strategies available to treat stroke are very limited. There is an urgent need to develop novel therapeutics that can effectively facilitate functional recovery. The injury that results from stroke is known to induce neurogenesis in penumbra of the infarct region. There is considerable interest in harnessing this response for therapeutic purposes. This review summarizes what is currently known about stroke-induced neurogenesis and the factors that have been identified to regulate it. Additionally, some key studies in this field have been highlighted and their implications on future of stroke therapy have been discussed. There is a complex interplay between neuroinflammation and neurogenesis that dictates stroke outcome and possibly recovery. This highlights the need for a better understanding of the neuroinflammatory process and how it affects neurogenesis, as well as the need to identify new mechanisms and potential modulators. Neuroinflammatory processes and their impact on post-stroke repair have therefore also been discussed.

Keywords: Cytokines; Neurogenesis; Neuroinflammation; Stroke; Stroke therapy.

Fig. 1

Schematic representation of adult neurogenesis in rodents. a Healthy brains: Neural stem cells proliferate from the SVZ and SGZ form neuroblasts that migrate to the olfactory bulb and local parenchyma. b Stroke brains: There is pronounced loss of striatal and cortical neurons, giving rise to increased proliferation of progenitors. The neuroblasts formed before and after the stroke migrate to the site of injury, influenced by chemokines and cytokines secreted by resident and activated microglia, reactive astrocytes, etc. The neuroblasts then differentiate into newborn neurons coupled with angiogenesis at the site of injury, giving rise to mature neurons