Evaluation of anti-alzheimer activity of ethanolic and methanolic extracts of Polygonum Glabrum against Aluminum chloride induced Alzheimer’s in experimental rats
Background: Human clinical trials seek to ameliorate the disease states and symptomatic progression of illnesses that, as of yet, are largely untreatable according to clinical standards. Ideally, clinical trials test “disease-modifying drugs,” i.e., therapeutic agents that specifically modify pathological features or molecular bases of the disease and would presumably have a large impact on disease progression. In the case of Alzheimer’s disease however, this approach appears to have stalled progress in the successful development of clinically useful therapies. For the last 25 years, clinical trials involving Alzheimer’s disease have centered on beta-amyloid and the hypothesis of Alzheimer’s disease progression and pathology. Aim: The current study aimed at investigation of effectiveness of ethanolic and methanolic extract of Polygonum glabrum in Aluminum chloride induced Alzheimers disease in experimental rats. Methods: The behavioral parameters evaluated by following methods like, Morris water maze Test, Radial arm maze Test, Active avoidance Test. Biochemical parameters were also estimated like Acetyl choline and Acetyl choline esterase. Results: Polygonum glabrum extract was instituted to be neuroprotective against AlCl3 induced toxicity. Enhanced learning and memory were allied to ingestion of extract in rats. Al overload, AChE hyperactivity is responsible for Alzheimer’s disease which are neutralized or reduced with treatment of extract, which might be due to the synergistic action of its active constituents. Ethanolic extract was shown slightly higher efficacy as compared to methanolic extract Conclusion: Based on these current findings, it is suggested that lowering Aβ is an unproven strategy, and it may be time to refocus on other targets for the treatment of this disease including pathological forms of tau.
Keywords: Alzheimer’s disease, beta-amyloid plaque, Aβ peptide.
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