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Compelling evidence demonstrates that molecular change characteristics for AD, such as oxidative stress and amyloid <jats:italic>\u03b2<\/jats:italic> (A<jats:italic>\u03b2<\/jats:italic>) oligomerization, precede by decades the onset of clinical dementia and that the disease represents a biological and clinical continuum of stages, from asymptomatic to severely impaired. Nevertheless, the sequence of the early molecular alterations and the interplay between them are incompletely understood. This review presents current knowledge about the oxidative stress\u2010induced impairments and compromised oxidative stress defense mechanisms in AD brain and the cross\u2010talk between various pathophysiological insults, with the focus on excessive reactive oxygen species (ROS) generation and A<jats:italic>\u03b2<\/jats:italic> overproduction at the early stages of the disease. 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