Abstract: AD is a multifactorial and multifaceted disease, with a complex and still not completely understood pathogenesis (Cervellati et al., 2016; Iturria-Medina et al., 2016). Multiple hypotheses have been proposed to explain the pathobiology of the disease. In this plethora of mechanistic models, the central role amyloid beta (Aβ) forming neuritic plaques remains undiscussed. However, the adjective “central” does not mean that Aβ alone can trigger and fuel all the AD neurodegenerative process. Indeed, it is now amply recognized that a combination of multiple biochemical (especially redox), immune system and vascular abnormalities must also occur to define the direction of disease trajectory (Iturria-Medina et al., 2016). This complexity is probably one of the main reasons for the current unavailability of disease-modifying therapies that may prevent or slow the rate of disease progression.