Nonsteroidal anti-inflammatory drugs (NSAIDs) have been considered for the treatment and prevention of Alzheimer’s disease (AD) for more than two decades. The rationale for this approach is derived from epidemiological studies and from the observation that the causative amyloid pathology in the AD brain is accompanied by a secondary inflammatory response. Given that the primary pharmacological targets of NSAIDs are cyclooxygenases (COX), the reduced expression of inflammatory markers in AD mouse models after peripheral administration of NSAIDs has suggested that these compounds may be beneficial in AD by inhibiting a wide range of inflammatory responses in the central nervous system.