Background: Number of contradictory reports are available on the effects of antiinflammatory
drugs on Alzheimer’s disease (AD) including beneficial, adverse and stage dependent
effects. We provide insights of the effects exerted by some anti-inflammatory drugs
on the chemistry of AD.
Methods: Three different doses of dexamethasone (0.015, 0.030, 0.060 μM), piroxicam (5,
7.5, 10 μM), indomethacin (1, 1.25, 1.50 μM), diclofenac (0.6, 0.8, 1.0 μM), aspirin (90, 120,
150 μM) and celecoxib (30, 45, 60 μM) were used. Rivastigmine, methylene blue and butylated
hydroxyanisole were used as standard drug, oligomerization inhibitor and antioxidant,
respectively. Oligomerization and fibrillization reactions were performed using Aβ1-42 peptides.
Results-Indomethacin and aspirin mainly inhibited oligomerization, while rivastigmine
and piroxicam inhibited fibrillization. Diclofenac and celecoxib inhibited both oligomerization
and fibrillization almost equally. Dexamethasone showed poor efficiency on both the
processes, but exert comparably more inhibition of oligomerization than fibrillization. Inhibition
of acetylcholinesterase activity was also potent and was in the following order: celecoxib>
piroxicam> diclofenac> aspirin> indomethacin> dexamethasone. Strong radical scavenging
(More than 50%) activity was showed by indomethacin and aspirin for NO radicals.
Conclusion: Present study consistently revealed that anti-inflammatory drugs have potential
to Modulate chemistry of AD progression. Inclusion of anti-inflammatory drugs in low doses
along with routine therapies may provide therapeutically and economically more efficient
therapies for AD. However, further studies are warranted, because the overall therapeutic effect
seems to be the function of stage of disease, dose of drug, main underlying mechanism of