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ABSTRACT
Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease. It is the most common type of dementia characterized by a progressive deterioration in cognition as well as a decline in activities of daily living together with behavioural changes. Despite decades of research there is currently no cure for Alzheirmer’s disease and available treatments only provide limited symptomatic relief. Objective: The aim is to assess the effect of the administration of NAcetylglucosamine(GlcNAc) treatment on the expression Brain derived neutrotrophic factor (BDNF) and glycogen synthase kinase 3B(GSK3B) expression in the cerebellum and cortex in a scopolamine induced Alzheirmer’s disease-like condition in a mouse model comparing it with Donepezil, a standard Alzheimer’s disease treatment. Methods: Fifty-five female Swiss albino mice were divided into eleven groups, five for the preventive group and six for the curative group. The groups received either distilled water, various doses of N-Acetylglucosamine or Donepezil orally for 14 days. Scopolamine was administered to induce an Alzheirmer's disease-like condition. Gene expression analysis of glycogen synthase kinase 3 and brain derived neutrotrophic factor in the cerebellum and cortex was then conducted. Results: N-Acetylglucosamine treated groups demonstrated significant increase in the expression of brain derived neutrotrophic factor in both cerebellum and cortex compared to the control group for both preventive and curative groups. However, there was a significant decrease in the expression of glycogen synthase kinase 3B in both cerebellum and cortex when compared to the control groups in both preventive and curative groups suggesting a potential mechanism for Alzheirmer’s disease treatment. Conclusion: N-acetylglucosamine administration exhibited promising therapeutic benefits by improving brain derived neutrotrophic factor gene expression and reducing glycogen synthase kinase 3B expression in an Alzheirmer’s disease like condition. These findings highlight the potential significance of GlcNAc as a treatment option for Alzheirmer’s disease.
