A neuropathological characteristic of Alzheimer's disease is the extracellular accumulation of amyloid beta peptide (Abeta) in neuritic plaques. Recent evidences suggested that soluble Abeta oligomers are the predominant neurotoxic species for neurons. Thus, considerable attention has been paid to discriminate the cytotoxic pathways of Abeta pre-fibrillar aggregates and mature fibrils. We showed that the mechanisms by which Abeta oligomers and fibrils generated reactive oxygen species differ in terms of site of production and kinetics, suggesting the involvement of different intra/extracellular pathways.
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