β-amyloid, the 39-43 amino acid peptide fragment originating from amyloid precursor protein, is today, generally accepted as the biological entity responsible for causing the debilitating human disorder Alzheimer's disease. Understanding the exact biological effects of β-amyloid in vitro and in vivo is clearly important to provide therapeutic strategies for the disease. Recent in vitro studies have focused on the production of reactive oxygen species by aggregating β- amyloid, but the cellular effects of β-amyloid induced reactive oxygen species production have not been fully elucidated.