Deposition of amyloid beta-protein in the brain has been regarded as the central event in Alzheimer's disease; however, amyloid beta-protein precursor is an endogenous protein, probably with neurotrophic functions. An alternative hypothesis is that amyloid beta-protein is involved in the disease process secondarily, as a protective reactant when brain cells are injured. Insufficiency of amyloid beta-protein precursor, whether because of a genetic defect or in relation to the action of environmental factors, then allows development of Alzheimer changes.