ABSTRACT
A growing body of data suggest that free radicals are involved at some point in the pathogenesis of Alzheimer’s disease (AD). However, most studies regarding the role of oxidation in AD are being conducted in vitro. Although such ap proaches are expedient, the results are often difficult to correlate with the se quence of events that characterize the course of the human disease. One of the main reasons for this problem is that in vitro models do not reflect well the complexity of the stress response in nervous tissue. Induction of heat-shock pro teins in tissue glia, for example, is followed by export of the proteins into adjacent axons so that compartments that are distant from the neuronal soma can be effec tively protected (1). Such intricate interactions are ideally studied only in in vivo paradigms.
