Cognitive dysfunction, one of the most striking age-related impairments seen in human beings, has been correlated to the vulnerability of the brain to increased oxidative stress during aging process.
Quercetin is a
bioflavonoid with strong
antioxidant properties. Experiments were performed to study the possible effects of
quercetin on cognitive performance of young, aged or
ethanol-intoxicated mice (an animal model for cognition dysfunction) using one trail step down type of passive avoidance and elevated plus maze tasks, respectively. Aged or chronic
ethanol-treated mice showed poor retention of memory in step-down passive avoidance and in elevated plus-maze task. Chronic administration of
quercetin (10, 25 and 50 mg/kg) for 30 days or its co-administration with
ethanol (15% w/v, 2g/kg per orally) for 24 days significantly reversed the age-related or chronic
ethanol-induced retention deficits in both the test paradigms. However, in both memory paradigms chronic administration of
quercetin failed to modulate the retention performance of young mice. Chronic
quercetin administration for 30 days also reversed age associated increase in
TBARS levels and decline in forebrain total
glutathione (GSH), SOD and
catalase levels. Chronic
ethanol administration to young mice produced an increase in lipid peroxidation, and a decline in forebrain total
glutathione (GSH), SOD and
catalase levels, which was significantly reversed by the co-administration of
quercetin (10, 25 and 50 mg/kg). The results of the present study showed that chronic
quercetin treatment reverses cognitive deficits in aged and
ethanol-intoxicated mice, which is associated with its
antioxidant property.