The more reliably identifiable prodromal phase of dementia with Lewy bodies than Alzheimer’s disease provides a critical opportunity for intervention

There is a great deal of evidence suggesting a fundamental role of central and peripheral inflammation in the pathogenesis of Alzheimer’s disease (AD).1 Neuropathological and neuroradiological studies have indicated that activated microglia and inflammation-related mediators is observed in the cerebral neocortex of patients with early AD before extensive tau-related neurofibrillary pathology develops. Numerous epidemiological studies have revealed that treatment with non-steroidal anti-inflammatory drugs decreases the risk for developing AD. However, several prospective clinical trials showed no benefit from anti-inflammatory drugs in patients with symptomatic AD. These results imply that therapies should be initiated during earlier stages of AD pathology. Although it has been established …