The amyloid β peptide (AβP) is a small fragment of the much larger, broadly distributed amyloid precursor protein (APP). Abundant AβP deposition in the brains of patients with Alzheimer's disease suggests that altered APP processing may represent a key pathogenic event. Direct protein structural analyses showed that constitutive processing in human embryonic kidney 293 cells cleaves APP in the interior of the AβP, thus preventing AβP deposition. A deficiency of this processing event may ultimately prove to be the etiological event in Alzheimer's disease that gives rise to senile plaque formation.