The aim of this article is to review the role of mitochondria in the pathogenesis of Alzheimer's disease. Additionally, the effect of gender on the incidence of Alzheimer's disease and the pathophysiological mechanisms involved will be discussed. Mitochondria, in the presence of Alzheimer's amyloid-beta peptide, increase the formation of reactive oxygen species which act both as damaging agents and also as signaling molecules. These radicals, in fact, unleash a mechanism involving the liberation of cytochrome c that leads to neuronal apoptosis. Notably, young females appear protected against the mitochondrial toxicity of amyloid-beta, likely due to the upregulation of antioxidant enzymes which occur in females. Estrogens are responsible for this effect. Overall, the findings support the notion that amyloid-beta causes intracellular toxicity via the increased production of oxidant species. Reactive oxygen species generated by mitochondria act as a signal to start the mitochondrial apoptotic pathway. There is a possibility of prevention, and indirect evidence shows that estrogenic compounds (either endogenous estradiol or phytoestrogens such as genistein) may increase the expression of antioxidant enzymes, leading to a lowering of oxidative stress and thus protection against intracellular toxicity of amyloid-beta peptide. These ideas open up the possibility of using phytoestrogens to prevent the onset of Alzheimer's disease. More studies are required to determine whether estrogens and/or phytoestrogens fulfill these expectations.