THE RECENTLY completed "Decade of the Brain" witnessed fundamental advances in many areas of basic and clinical neurosciences, but few fields experienced greater progress than those dealing with Alzheimer disease (AD). Mutations in the amyloid precursor protein (APP), presenilin 1 (PS1) , and presenilin 2 (PS2) genes that result in autosomal dominant familial AD were identified in the early part of the decade.1 These discoveries made possible the development of transgenic animals,2 which provide the best available experimental models to study AD neuropathology and therapeutics. More recently, the enzymes involved in processing APP, β-secretase, and probably γ-secretase (which may turn out to be PS1), have been identified, and specific inhibitors of these proteases have been developed and are nearing or undergoing clinical trials. Furthermore, much has been learned about inflammatory reactions in brain tissue during the course of AD,3 and both epidemiologic and animal model–based experimental observations suggest that anti-inflammatory4,5 or immunological strategies6 may be effective in ameliorating this devastating disease. Clinical trials testing these therapies are under way.