الفهرس 
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Abstract
Alzheimer’s disease is a neurological disease that causes death of nerve cells. The aim of the present study was to investigate the possible underlying mechanisms of neuroprotection of dapagliflozin against AlCl3 induced AD in rats. AlCl3 caused cognitive decline. Dapagliflozin was able to improve learning abilities in rats and significantly lower Aβ, AChE levels, and OS markers. It was also found that dapagliflozin had the potential to enhance brain glucose metabolism. Furthermore, dapagliflozin caused an upregulation in the expression of AMPK/mTOR pathways as well as HO-1. Thus, treatment with dapagliflozin demonstrated a strategy for protecting the brain from the deteriorating effects of AlCl3.
Keywords: Alzheimer’s disease, dapagliflozin, AMPK pathway, oxidative stress, glucose metabolism.