An abnormality of plasma amyloid protein precursor in Alzheimer's disease

Abstract

βA4 amyloid deposition in the brain, which is characteristic of Alzheimer's disease(AD), may result from either overexpression of the amyloid protein precursor (APP) or failure of APP to be correctly processed. A blood marker reflecting this abnormal metabolism would be of diagnostic value and would provide a means of monitoring the efficacy of therapeutic interventions. We analyzed immunoblots of plasma APP enriched by heparin‐Sepharose chromatography from patients with moderate to severe AD dementia (n = 34) and control subjects (n = 77) and found an approximately 50% increase in the proportion of 130‐kd APP species in patients with AD (p < 0.001), no difference in the 110‐kd form, a 15 to..