The pathophysiology of Alzheimer's disease (AD) includes the deposition of amyloid beta protein (Abeta) and the ensuing initiation of a variety of secondary processes, including tau hyperphosphorylation, excitotoxicity, oxidation, and inflammation. Nerve cell loss in structures responsible for manufacturing neurotransmitters results in a variety of neurochemical deficits. Current therapeutic approaches to the treatment of AD include cholinesterase inhibitors for mild to moderate disease, memantine for moderate to severe disease, and vitamin E or selegiline. Reduction of Abeta generation or aggregation, enhancement of Abeta removal, interruption of tau hyperphosphorylation, and the use of more efficacious antioxidant or anti-inflammatory agents represent promising therapeutic strategies currently being investigated. Improved methodologies for clinical trial design and analysis and the development of biological markers may hasten the identification of effective treatments for AD.