الفهرس 
AcknowledgmentOnly 14 pages are availabe for public view
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Abstract
Alzheimer’s disease (AD) is a neurodegenerative disease characterised by the presence of β-amyloid (Aβ) plaques and acetylcholine depletion leading to neurobehavioral defects. AD was contributed also with downregulation of TGF-β1/SMAD2 and GSK-3β/β-catenin pathways. Simvastatin (SMV) improved memory function experimentally and clinically. Hence, this study aimed to investigate the mechanistic role of SMV against aluminium chloride (AlCl3) induced neurobehavioral impairments. Treatment with SMV improved the memory deterioration induced by AlCl3 with significant recovery of the histopathological changes. This was concomitant with the decrease of AChE and Aβ (1- 42). SMV provides its neuroprotective effect through upregulating the protein expression of β-catenin, TGF-β1 and downregulating the expression of GSK-3β, TLR4 and p-SMAD2.