Neuroprotective Potential of Fingolimod Against Aluminium Chloride Induced Experimental Dementia in Rats

Abstract

BackgroundAlzheimer’s disease (AD) is an age related neurodegenerative disease mainly characterized by progressive cognitive decline, synaptic loss, extracellular amyloid‐beta (Aβ) deposits and intracellular accumulation of neurofibrillary tangles of tau protein. Multiple etiological factors have been linked with AD pathophysiology, oxidative stress, neuroinflammation, neurotransmitter deficit and foremost are the deregulation of lipid metabolism, consistently involve in AD pathology and cognitive deficit. In the present study, we have explored the neuroprotective potential of Fingolimod (FTY720), against Aluminium Chloride (AlCl3) induced experimental dementia in the rats.MethodAlCl3 at the dose of (175mg/kg, p.o.) daily on first to 35th day. Spatial and non‐spatial memory was evaluated by using Morris water maze and object recognition test. Fingolimod (0.25 and 0.5 mg/kg, p.o.) was administered at weekly intervals after administered AlCl3 in rats. Administered AlCl3 in rats produced cognitive deficit and caused significant elevation in markers and oxidative stress and degenerative changes in hippocampus and cortical brain region.ResultOn the countatary, fingolimod treatment attenuate AlCl3 induced cognitive decline, reduced oxidative burden and able to preserve neuronal architecture and prevent neuronal loss in hippocampus and cortical brain region of the rats.ConclusionThe present study suggests that Fingolimod (FTY 720) show beneficial effects in treating dementia. Our data demonstrated that Fingolimod could be effective in the protection of toxicity induced by Aluminium chloride