Neuronal cell death results from various circumstances such as hypoxia, ischemic and neurodegenerative diseases (NDs). In these events, the resulting modification of neurotransmitters, either excitatory or inhibitory, mediate much of the neuronal damage. However, this consequence depends upon their pre and post synaptic receptor activities which are the key mechanism for signal regulation. Among these, acetylcholine (ACh) is a well known neurotransmitter which is predominantly involved in neuroprotection as well as cognitive functions through its receptors activity, particularly the nicotinic subtypes. Several lines of evidence suggest that among these subtypes, a7 nicotinic acetylcholine receptor (a7nAChR) offers much promise for neuroprotective role in relation to the central nervous system (CNS) disorders like schizophrenia and Alzheimer's disease (AD). Several lines of evidence exist to show the potential mechanisms in which this nAChR subtype and its agonists such as nicotine, that trigger the a7nAChR-mediated suppression of neuronal cell death. This review focuses on the potential role of a7nAChR in neuroprotection by examining recent experimental data, both in vitro and in vivo, that argue for the neuroprotective role of a7nAChR in the CNS.