While the exact causes or mechanisms of Alzheimers disease (AD) are still not known, the most critical risk factor is aging. Cellular oxidative stress is known to occur in the brain during aging and some pathology of AD could be explained by the oxidative stress, including senile plaques, deposition of amyloid peptide (Aβ) and tangles (deposition of an abnormally phosphorylated tau). Also gliosis, which may release inflammatory molecules and cause oxidative stress, is a feature of aging and AD. Epidemiological analysis indicates that people with severe arthritis and who are subjected to leprosy therapy have significantly lower rates of AD. Since both arthritis and leprosy therapy involves high doses of nonsteroidal anti-inflammatory drugs (NSAIDs), and the fact that inflammation is involved in AD pathology, NSAID-therapy might prevent or delay the onset of AD. More recently NSAIDs were found to reduce production of Aβ peptide. Therefore, we should revisit NSAIDs as potential treatment for AD therapy. There are clinical studies showing the beneficial effects of NSAIDs treatments in AD patients, in contrast, other studies show a lack of benefit. This article discusses the role of inflammation and oxidative stress in AD and the role of drugs preventing them.