Effects of Age and Amyloid Deposition on Aβ Dynamics in the Human Central Nervous System

Abstract

The Aβ peptide has been implicated as a critical initiator of Alzheimer disease (AD).1 Pathologic studies of the brain tissue of patients with AD demonstrate that extensive amyloid plaques associated with the disrupted neuropil are deposited throughout the cortex. Aβ peptides are the primary component of amyloid plaques, which account for a 1000-fold increase of Aβ in the AD brain. Increased brain Aβ in AD has been postulated to be caused by increased Aβ production or decreased clearance.2,3 Thus, the study of Aβ levels in individuals with AD is likely to lead to a better understanding of AD pathophysiological changes as well as normal Aβ physiology.