Translational Stroke Research

Abstract

Delayed neuronal death in the penumbral region of a stroke is largely responsible for many negative implications seen in stroke victims. This type of neuronal death occurs in many forms, including apoptosis, necrosis, and alternative mechanisms. Although caspases are usually associated with apoptosis, there are several morphologically and biochemically distinct types of cell death that are independent of caspase activation. Downstream effectors and processes of mitochondrial damage, such as AIF, endonuclease G, BNIP3, mitophagy, mitochondrial biogenesis, chaperone-mediated autophagy, reactive oxygen species production as well as parallel endoplasmic reticular stress and lysosomal dysfunction, have all been shown to play a role in post-stroke delayed neuronal cell death. In this chapter, we attempt to summarize these caspase-independent events and their potential therapeutic applications as targets for intervention.