AbstractBackgroundAlzheimer’s disease (AD) is an age related progressive neurodegenerative disorder mainly characterized by cognitive decline, synaptic loss, and other mental functions. Extracellular amyloid beta (Aβ) deposits and intracellular accumulation of neurofibrillary tangles of tau protein are the two major hallmarks of AD. Multiple etiological factors have been linked with AD pathophysiology, oxidative stress, neuroinflammation, neurotransmitter deficit and foremost are the dysregulation of lipid metabolism, consistently involve in AD pathology and cognitive deficit.MethodIn the present study, we have explored the neuroprotective potential of Fingolimod (FTY720), against Aluminium Chloride (AlCl3) induced experimental dementia in the rats. AlCl3 at the dose of 175mg/kg, p.o was given daily from 1st to 35th day. Spatial and non‐spatial memory was evaluated by using Morris Water Maze (MWM) and Object Recognition Test (ORT). We further performed biochemical tests to check the levels of different oxidative stress markers.ResultAdministered AlCl3 in rats produced cognitive deficit and caused significant elevation in markers of oxidative stress and showed degenerative changes in hippocampus and cortical brain region. On the contrary, fingolimod treatment attenuate AlCl3 induced cognitive decline, reduced oxidative burden and showed potential of restoring neuronal architecture and prevent neuronal loss in hippocampus and cortical brain region of the rats. The present study suggests that Fingolimod (FTY720) show beneficial effects in treating dementia.ConclusionOur data demonstrated that Fingolimod could prove to be a beneficial therapeutic target in the protection of neurotoxicity induced by Aluminium chloride and help in improving memory and other cognitive functions.