Alzheimer´s disease (AD) is characterized by extensive neuronal loss in brain areas related to memory and cognitive functions. Central to the neurodegenerative process is a peptide termed Abeta. The latter is the main component of senile plaques, one of the histopathological hallmarks of AD, and derives from proteolytic processing of the Alzheimer´s amyloid precursor protein (APP). Among the alterations induced by Abeta is increased cellular oxidative stress, imbalanced protein phosphorylation and cytoskeletal abnormalities, all factors that contribute to neuronal death.