Determining the incidence and prevalence of dementia is an inexact science. Dementia is difficult to define and detect in the population. Even with the difficulties of determining prevalence and incidence, it is clear that dementia causes a substantial burden on our society. Problems with diagnostic inaccuracy and insidious disease onset influence our ability to observe risk factor associations; factors related to survival may be mistaken for risk/protective factors. Current studies suggest that factors influencing brain development or cognitive reserve may delay the onset of AD, perhaps through a protective mechanism or a delay in diagnosis caused by improved performance on cognitive tests. The recent identification of genes that cause dementia suggests that these genes or their biochemical pathways may be involved in the pathogenesis of nonfamilial cases. The contribution of genes that cause disease in and of themselves may be smaller than that of genes that act to metabolize or potentiate environmental exposures. The interaction between gene and environment should be increasingly well studied in the future. Epidemiology must take advantage of these molecular advances. The tasks of public health and epidemiology should still involve prevention, the nonrandom occurrence of disease, and its environmental context in addition to heredity. The tools to address these tasks should continue to be refined.