Chronic stress has been known to cause numerous changes in brain structure that include alter its neurochemistry, excitability, neuronal morphology and cell death (Conrad, 2006). Oxidative stress and reactive oxygen species are known to play a crucial role in the progression of stressinduced neurological diseases (Kontos and Wei, 1986). Production of free radicals after chronic unpredictable stress plays a key role in the pathogenesis of cognitive deficits (Farooq et al., 2012). Traumatic brain injury releases pro-inflammatory cytokines and results into neuroinflammation in hippocampus and other brain parts, leading to cognitive imbalance (Kontos and Wei, 1986). Oxidative damage and apoptosis are two crucial mechanisms that play a significant role in traumatic brain injury-induced neurological disorders (Bayir et al., 2003). Chronic stress is also known to increase serum corticosterone level and impairs memory retrieval process (Kurukulasuriya et al., 2004). Olfactory bulbectomy alters neurogenesis in several regions of brain, which is one of the putative pathogenic mechanisms to explain depression like state (Koo et al., 2010). The several neurodegenerative diseases associated with chronic stress mostly includes depression and memory dysfunction (Radley et al., 2004). All these forms of chronic stress are known to cause oxidative damage, mitochondrial dysfunction, neuroinflammation, and apoptosis with significant alterations in behaviour parameters (Halliwell, 2006). However, the molecular and cellular mechanism and pathways associated with these stress related problems are still not known and poorly understood.
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