In medical science, brain is among the most dominated complex structure in the humans. It is made up of neurons and neuroglia, the neurons being responsible for sending and receiving nerve impulses or signals. It is assumed that neuroglial activation is largely determined by neuronal signals.( Halliwell, 1992),(Kumar and Khanum, 2012). It is known that brain pathology in the form of cerebrovascular and neurological disease is a leading cause of death all over the world, with an incidence of about 2/1000 and an 8% total death rate in 1995 (Kolominsky et al., 1998).  A neurological disorder is any disorder of the nervous system. Structural, biochemical or electrical abnormalities in the brain, spinal cord or other nerves can result in a range of symptoms. There are more than 600 neurologic diseases – epilepsy, dementia, parkinson’s. According to Global Burden of Disease (GBD) study, a collaborative endeavour of the World Health Organization (WHO), by 2030 neurological disorders among human community becomes one of the leading causes of death especially in developing and under developing countries (WHO 2006). Developing countries, including India are passing through a phase of epidemiological transition with increasing burden of non-communicable diseases (NCD) consequent to transformation of scenario with improvement of health care services in preventive and promotive domains. Among the NCDs, neurological disorders form a significant proportion of global burden of disease (M Gourie-Devi). The GBD presented the data and estimated the neurological disorders for 2005, 2015 And 2030. Neurological disorders included in the neuropsychiatric category contribute to 2% of the global burden of disease, while cerebrovascular disease and some of the neuroinfections (poliomyelitis, tetanus, meningitis and Japanese encephalitis) contribute to 4.3% of the global burden of disease.Neurological disorders are an important cause of mortality and constitute 12% of total deaths globally by 2030. The DALY’s (Disability Affected Life Years) with neurological disorders for 2005, 2015, 2030 are presented in the Table 1.1 (WHO, 2004). Neurological disorders contribute to 92 million DALY’s in 2005 projected to increase to 103 million in 2030 (approximately a 12% increase) and death attributable to neurological disorders are mentioned in Fig. 1.1.The impact of neurological disorders also depends on the total income category of the person which is shown in Fig. 1.2 Thus, there is seriously a need of protective agents to treat the several neurological disorders and such agents are called as neuroprotective agents or neuroprotectants. Neuroprotection is defined as the ability for a therapy to prevent neuronal cell death by intervening in and inhibiting the pathogenic cascade that results in cell dysfunction and eventual death (Anthony et al., 2009).1.2 Pathogenesis of neuronal damage and cell death Two important processes that lead to irreversible neuronal damage are outlined below.-1.2.1 Rapid necrosis (chaotic cell death)Interruption of blood/oxygen supply to the brain results in dysfunction of ATP dependent ion channels, leading to cellular depolarization and the release of extracellular excitatory neurotransmitters like glutamate. Glutamate activates the N-methyl-D-aspartate (NMDA) receptor subtype of glutamateric receptors. Activation of NMDA receptors increases intracellular calcium and sodium, contributing further to depolarization and neuronal activation. Excess calcium promotes activation of pathways which upset ionic homeostasis, nitric oxide signaling, cytoskeleton function, free radical generation, and protease and lipid activation, ultimately leading to membrane degeneration and excitotoxic cell death (Sanders  et al., 2005)1.2.2 Delayed apoptosis (programmed cellular death)Necrosis and apoptosis are accompanied by an array of other processes which lead to Neurodegeneration (Polster et al., 2004). These include-1.2.2.1 An immunologic (inflammatory) responseRelease of cytokines, such as tumor necrosis factor and interleukins, is mediated by oxidative stress. The significance of the immunologic response is not entirely clear, because it exacerbates oxidative stress on one hand and promotes the removal of dead neurons and neurogenesis on the other (Coimba et al., 1996).1.2.2.2 Oxidative stressOxidative stress is also a feature of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and amyotrophic lateral sclerosis. The brain has a high rate of oxygen consumption, making it susceptible to oxidative stress secondary to the formation of excessive free radicals, which lead to direct tissue damage and stimulate inflammatory and pro-apoptotic cascades (Wang etal, 2006).1.2.2.3 Massive extracellular catecholamine releaseCentral norepinephrine release during brain ischemia increases neuronal metabolism (increases cerebral metabolic rate for oxygen, leads to the formation of free radicals from auto-oxidation of neurotransmitters, such as norepinephrine and dopamine, and exacerbates damage caused by glutamate during ischemia (Ellen et al., 2006).1.3 Features of an ideal neuroprotectantIf an ideal neuroprotectant drug were to be developed, one needs first to consider a simple list of what desirable features of the ideal neuroprotectant drug might be. These must include-(i) Effectiveness pre-ischemia (Gabryel et al., 2012) and posthoc, thus enlarging the window of opportunity for neuroprotective intervention.(ii) A simple route of administration; ideally- orally.(iii) Rapid onset of action(iv) Must possess restorative property.(v) A high tolerability and a low side-effect profile.1.4 Pharmacological strategies and agents for neuroprotection1.4.1 Free radical scavengersFree radicals, especially superoxide (O(2)*-), and non-radicals, such as hydrogen peroxide (H2O2), can be generated in quantities large enough to overwhelm endogenous protective enzyme systems, such as superoxide dismutase (SOD) and reduced glutathione (GSH) (Slemmer et al., 2008). Several free radical scavengers have been developed and some of them have progressed into clinical trials. One of them, edaravone, has been approved by the regulatory authority in Japan for the treatment of stroke patients.(Wang et al., 2007) The ceria(Chung, 2003) and yttria (Bloor et al., 1994) nanoparticles act as direct antioxidants to limit the amount of reactive oxygen species required to kill the cells and this group of nanoparticles could be used to modulate oxidative stress in biological systems. 

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