Limiting Functional Deficiency Following Stroke: Exploiting Different Stem Cell Reservoirs

Stroke is the third leading cause of death after cancer and heart disease. Although great strides have been made in our understanding of the mechanisms that contribute to stroke pathology, effective pharmacological interventions for the millions of people annually affected by this disease is minimal. The only available treatment is tissue plasminogen activator (tPA) which promotes reperfusion of the ischaemic area, but the high associated risk of bleeding and short effective window have severely limited its use. Historically, much research to identify new therapeutics for the treatment of stroke has focussed on the mechanisms that promote cell death within the brain during and immediately after the traumatic event. Drugs that disrupt these mechanisms and thereby prevent cellular damage in animal stroke models have, unfortunately, proven disappointing in the clinic. A potentially more effective way of managing patients would be to target events that contribute both to the cellular damage and the tissue repair that occurs some time after the initial trauma. This review describes our current understanding of the mechanisms involved in later stage damage and, particularly, those processes that contribute to cellular and, therefore, functional recovery within injured areas of the brain. Potential strategies for exploiting these processes to achieve better and faster recovery of the patient will then be discussed.