Nelonemdaz, a promising breakthrough neuroprotectant for the treatment of stroke

Abstract

Byoung Joo Gwag

Neuronal and glia cells undergo widespread degeneration over time following stroke attack, which results in devastating neurological deficits. Cellular and molecular mechanisms have been delineated underlying pathological brain cell death. Accumulation of extracellular glutamate can cause fulminant neuronal death through excess activation of N-methyl-D-aspartate (NMDA) receptors and subsequent calcium overload after ischemic brain injury. In addition, free radicals contribute to slowly evolving brain cell death after ischemic-reperfusion brain injury. Timely administration of NMDA antagonists and antioxidants significantly prevented brain cell death and functional deficits in preclinical studies. Unfortunately, more than 200 clinical trials of neuroprotectants including NMDA receptor antagonists and antioxidants had failed in showing beneficial effects for acute ischemic stroke patients

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