Cancer Stem Cell: The Seed of Tumors?

Abstract

Excitotoxicity is one of the central processes in cerebral ischemia, and is of great importance in the pathophysiology of both stroke and global ischemia. In this review, we have attempted to tackle the structural and functional changes to NMDAR after ischemia and explore the different roles NMDAR sub-units play in cerebral ischemia. Other associated pathologic processes, such as inflammation, apoptosis, and necrosis, will undoubtedly influence and overlap with excitotoxic pathways, and may result in further alterations to NMDAR structure and mechanisms. As research illuminates the pathway to NMDAR-mediated excitotoxic damage and neuroprotection, we hope that this will be followed by emergence of treatment of important conditions like stroke. Already, attempts have been made to prevent pro-death cascades by inhibiting NMDAR signaling at the level of the PSD, thus sparing any neuroprotective action stimulated by receptor activation. We hope that these and other therapies will prove that the elusive concept of neuroprotection is not a myth.