AbstractAlzheimer's disease (AD) is a growing serious public health problem worldwide. Clinically, AD is a progressive neurodegenerative disorder characterized by a global cognitive decline. There is significant evidence that reactive oxygen species‐mediated reactions, particularly of neuronal lipids, are extensive in those AD brain areas directly involved in the disease processes. Traditional views claim that oxidative‐mediated tissue injury in the AD brain is the result of neurodegeneration. In recent years, numerous investigations have pointed to the functional importance of oxidative imbalance as a crucial event in mediating AD pathogenesis. The availability of specific and sensitive markers to monitor in vivo oxidative imbalance, in combination with studies performed in living patients with clinical diagnosis of AD, are helping to elucidate these issues. Here, I summarize some of the most recent research on the relevance that oxidative imbalance and lipid peroxidation have in AD. The evidence accumulated so far clearly indicates that oxidative imbalance is an early event during the evolution of this devastating disease. This new concept implies that this phenomenon may play a more important role in AD pathogenesis than previously anticipated. Drug Dev. Res. 56:446–451, 2002. © 2002 Wiley‐Liss, Inc.