Lymphocyte Oxidative DNA Damage and Plasma Antioxidants in Alzheimer Disease

Abstract

A LARGE body of research suggests that oxidative stress, a condition representing an imbalance between oxidants and antioxidants in favor of the oxidants,¹ plays an important role in the pathogenesis of Alzheimer disease (AD).² The brain is particularly susceptible to the attack of free radicals caused by its low content of antioxidants, by the considerable content of polyunsaturated fatty acid side chains of the neuronal membrane lipids, and by its high oxygen consumption rate.^2,3 Furthermore, aging—a major risk factor for AD—is known to be associated with increased free radical production, and markers of oxidative DNA damage have been found to be increased in cerebral tissue of healthy aged subjects⁴ and even more so in patients with AD.⁵ The initial idea of a link between increased free radical production and AD⁶ is now supported by studies showing a potential vicious circle between free radical–induced β-amyloid formation and β-amyloid–related oxidative stress.⁷