Assessment of Ameliorative Effects of Choline on Neurodegeneration in Aluminium Chloride Induced – Alzheimer’s Disease Rat Model
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Abstract
Introduction: Alzheimer’s disease (AD), a common neurodegenerative disease of the elderly population is the most explored area of research in recent times owing to the dearth of successful treatment options for its reversal.
Objectives: To study the neuroprotective role of choline supplementation in comparison to AD therapeutic drug Donepezil in aluminium chloride induced Alzheimer’s disease rat model.
Methods: In the present study Group I served as the normal control. An attempt was made to induce AD in experimental rats by orally treating them with AlCl3 at a dose of 300mg/kg body weight (Group II) and observing the changes in parameters associated with various established hypothesis of the disease. Group III animals were treated with the standard drug, Donepezil (0.5 mg/kg body wt.). Choline, was supplemented in AD induced rats which were then monitored for the same parameters to demonstrate its role as neuroprotective agent prior to and post AlCl3 supplementation (Groups V & IV) respectively. The parameters studied in the brain homogenate included markers of AD pathology namely tau protein and caspase8, markers of cholinergic hypothesis namely acetyl choline, markers of oxidative stress namely MDA, reduced GSH and NO and marker of cognitive behaviour, water maze test. Additionally neuronal assay of prefrontal cortex and hippocampus was performed.
Results: Indicated that choline supplemented group (post treated) showed a significant decrease in tau protein compared to AM model; pre and post choline treatment showed a significant increase in GSH (p<0.05) and a significant improvement in cognitive behaviour (p<0.05) without significant changes in other parameters. Mean number of neurons in the CA1 region increased in choline treated groups IV and V compared to Al Cl3 treated group (Group1) wherein a drastic degeneration of neurons was observed.
Conclusions: Choline seemingly ameliorates the oxidative stress by significantly improving GSH status and the cognitive behaviour, significantly reduces the tau protein content in the brain and reverses the neuronal damage in the prefrontal cortex and hippocampus of rats treated with aluminium chloride.