Neuroprotection in stroke

Abstract

Stroke is a devastating disease affecting 15 million people worldwide and is the leading cause of adult disability (Circulation 121(7):e46-e215, 2010). Even where advanced technology and facilities are available, 60% of those who suffer a stroke die or become dependent (N Engl J Med 333(24):1581-1587, 1995). The introduction of thrombolytic agents and evolution of interventional strategies for recanalization have revolutionized the acute management of stroke (N Engl J Med 333(24):1581-1587, 1995). Despite this, a large number of strokes escape any acute intervention due to various contraindications or delay in presentation of the patient (Neurology 56(8):1015-1020, 2001). Even for patients who undergo acute therapy, ongoing secondary injury as a result of natural progression of the disease may cause progressive damage despite acute recanalization. This makes it pertinent to look for strategies to salvage all possible brain tissue irrespective of the use or success of acute stroke intervention. A variety of novel strategies to this effect are being investigated. Most of these originate from new knowledge of mechanisms of neuronal cell death and the new found concept of brain plasticity (Neuron 67(2): 181-198, 2010). Once considered exclusively a disorder of blood vessels, growing evidence has led to the realization that the biological processes underlying stroke are driven by the interaction of neurons, glia, vascular cells, and matrix components, which actively participate in mechanisms of tissue injury and repair. Yet despite success in animal and in vitro experiments, none of these strategies have yet been able to be applied to bedside clinical practice (Neuron 67(2): 181-198, 2010;