Abstract
Dementia is one of the age related mental problems and characteristic symptom of various neurodegenerative diseases including Alzheimer's disease. This impairment probably is due to the vulnerability of the brain cells to increased oxidative stress during aging process. Many studies have shown that certain phenolic antioxidants attenuate neuronal cell death induced by oxidative stress. The present work was undertaken to assess the effect of ethanolic extract of Punica granatum seeds on cognitive performance of aged and scopolamine treated young mice using one trial step-down type passive avoidance and elevated plus maze task. Aged or scopolamine treated mice showed poor retention of memory in step-down type passive avoidance and in elevated plus maze task. Chronic administration (21 days) of Punica granatum extract and vitamin C significantly (p < 0.05) reversed the age induced or scopolamine induced retention deficits in both the paradigms. Punica granatum extract also significantly lowered lipid peroxidation level and increased antioxidant glutathione level in brain tissues. Punica granatum preparations could be protective in the treatment of cognitive disorders such as dementia and Alzheimer's disease.
Highlights
With an increasing aging population, Alzheimer’s disease (AD) represents a significant healthcare issue, which is likely to gain in prevalence
Scopolamine induced cognitive deficit in second day was significantly reversed by pomegranate extract in young mice (Figure 1 B)
Chronic treatment of pomegranate extract and vitamin C significantly (p < 0.05) decreased the Transfer latency (TL) in aged and scopolamine treated young mice compared with respective controls (Figures 2A, 2B)
Summary
With an increasing aging population, Alzheimer’s disease (AD) represents a significant healthcare issue, which is likely to gain in prevalence. Recent reports suggest the involvement of free radicals in the pathophysiology of AD. Oxidative damage was considered a likely cause of age associated brain dysfunction because the brain is believed to be vulnerable to oxidative stress due to a relatively high rate of oxygen free radical generation without commensurate levels of antioxidative defenses (Brewer, 1998; Sohal et al, 1990). In AD, β-amyloid peptide has been implicated in oxidative stress and free radical production (Pappolla et al, 1997; Hardy and Higgins, 1992; Suh, 1997). Oxidative stress appears to mediate β-amyloid peptide toxicity by free radical production, suggesting a pathophysiological link between β-amyloid peptide and imbalance between reactive oxygen production and protective system
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