Abstract:
Aluminium metal (Al) has been implicated in etiology of many neurodegenerative
diseases, most commonly the Alzheimer’s disease (AD). Al causes the biochemical
defects, by affecting the neurotransmitters levels, causes conformational changes in
amyloid protein and increases amyloid accumulation in brain. There exists an
epidemiological linked between chronic exposure to Al and the incidence of AD.
Aim: This study was aimed at evaluating neuroprotective effect of Ibuprofen (IBU)
(25mg/kg/day for 12 days) in AlCl3induced
(150mg/kg/day for 12 days) toxicity.
Methods: Treated mice were subjected to learning and memory tests. Cholinergic
muscarinic receptors (mAChR; M1M5)
and APP isofroms (APP695, APP770 and
APP common) gene expression were carried out from the prefrontal
cortex area.
Results: Profound effect on learning and memory was observed in IBU treated
group along with enhanced expression of M1 mAChR (0.40±0.03; p<0.01)
compared to AlCl3inducedtoxicity
group (0.05±0.02). Fear memory was improved in
IBU treated group (89.68±2.58, p<0.01) as compared to AlCl3induced
toxicity
group (54.58±8.21). Discrimination index in social novelty test in IBU treated group
was improved (81.13±8.71; p<0.05), compared to AlCl3induced
toxicity group
(46.28±5.55).Similarly recognition memory of IBU treated group in novel object
recognition test was retained (66.85±5.60; p<0.05) compared to AlCl3induced
toxicity group (33.06±11.80). Conclusion: Ibuprofen demonstrated memory
enhancing effect, however, its effect on the APP isoforms expressions in prefrontal
cortex needs further studies.
