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Aim: To examine the protective outcome of quercetin against streptozotocin induced dementia in adult zebrafish. Materials and method: In this study, adult zebrafish (weighing 470-530 mg) were subjected to the streptozotocin administration (300 mg/kg; i.p) followed by a quercetin (50 & 100mg/kg i.p) pre-treatment before 24 hr of streptozotocin administration followed by blood glucose level measurement, behavioral parameters (light-dark test, novel diving test, open field test and T-maze test), biochemical parameters (lipid peroxidase, reduced glutathione, nitrite and AChEs activity), molecular and histopathological analysis. Results: In light-dark test, streptozotocin treated zebrafish shown their preference in dark compartment as compared to normal group. In novel diving tank, streptozotocin zebrafish spent less time and decrease in total number of entries to the top zone when compared to the normal group. In the T-maze test, streptozotocin treated zebrafish has shown significantly more time spent in unfavorable zone and less time spent in favorable zone with increase in total latency as compared to normal group. However, in the open field test no significant effect was seen among any group. Moreover, pre-treatment with quercetin (50 mg/kg and 100 mg/kg) significantly ameliorated the memory deficits in all the behavioral, biochemical and molecular parameters as compared to animals treated with streptozotocin. Additionally, results of histopathology studies showed less disruption in neuronal cells in quercetin treated group when compared to STZ treated animals.Conclusion: Pre-treatment with quercetin ameliorates streptozotocin induced dementia in adult zebrafish by preventing oxidative stress and neuroinflammation.

Stress is a common disorder affecting the normal functioning of the brain and behavior majorly in the prefrontal cortex and hippocampus region of the brain. Any long-term intrinsic and extrinsic stimulus evokes chronic stress-like conditions. Chronic stress reported enhancing the formation of reactive oxygen species, leading to mitochondrial cell death through the activation of the hypothalamic-pituitary axis which releases cortisol, excessive secretion of cortisol is responsible for alteration in glucose metabolism, and other neurological disorders such as anxiety, depression, multiple sclerosis, Alzheimer, and Parkinson’s disease. The purpose of this review is to provide an insight into the various pathophysiological aspects along with neurotransmitters involved in chronic stress and its association with various neurological disorders. Along with this, we also provided a background on the various experimental models of chronic stress.