Alzheimer's disease is a progressive degenerative disease with cognitive and behavioral manifestations. The pathophysiology of Alzheimer's disease is increasingly well understood, leading to approved and experimental therapies. Mutations on chromosomes 1, 14, and 21 can cause the disease and are sometimes present in patients with early onset Alzheimer's disease. Older patients--comprising the majority of Alzheimer's disease victims--have a variety of risk factors including age, gender, history of head trauma, low education level, and apolipoprotein genotype. The pathogenetic process leads to regional cell loss and biochemical deficits. The mutations and risk factors lead to increased amyloid production or accumulation and nerve cell death. Neurons atrophy in the cerebral cortex and in source nuclei of important neurotransmitters. The deficiency of acetylcholine can be partially remedied by cholinesterase inhibitors that produce modest cognitive and behavioral improvement. Anti-amyloid agents, antioxidants, anti-inflammatory drugs, estrogens, and calcium channel blockers may all slow the progression of Alzheimer's disease by interfering with specific steps within the disease cascade. Neuropsychiatric symptoms are also common in Alzheimer's disease and may be ameliorated by conventional psychotropic agents. Clinicians can currently offer substantial help to Alzheimer's disease patients, and the future promises more effective pharmacotherapy.