Alzheimer’s disease is one of the most serious neurodegenerative disorders occurring mainly in the old age. It results into memory and cognitive impairment leading to inability to perform routine tasks in day to day life and worsening of quality of life. Excitotoxic-neurodegeneration caused by over functioning of glutamatergic transmission is of the main pathophysiological aspects. Glutamate release is mainly mediated by sodium channels and blockade of these channels decreases the excessive release of this excitatory neurotransmitter. The present study evaluated Mexiletine, a sodium channel blocker established as an anti-arrhythmic agent, in progressive Alzheimer’s disease caused by excitotoxicity. Aluminum chloride, a well known neurotoxic compound, was administered at 100 mg/kg intraperitoneally for 45 days to induce Excitotoxic-neurodegeneration followed by memory impairment similar to Alzheimer’s disease. Mexiletine was administered in high and low doses of 85 mg/kg and 60 mg/kg both intraperitoneally in their respective groups continuously throughout the induction period. Memantine was selected as a standard drug and was administered similarly. Cognitive functions were checked by Step-down latency model and elevated plus maze model. Prolongation in step-down latency and shortening of transfer latency were observed in test and standard group animals indicating memory retention and the significant prevention of Alzheimer’s disease in treated animals. Further studies are going on to confirm the mechanism of action of Mexiletine in Alzheimer’s disease.
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