Alzheimer's disease (AD) is defined by the concurrence of accumulation of 
abnormal aggregates composed of two proteins: Amyloid beta (Aβ) and tau, and of 
cellular changes including neurite degeneration and loss of neurons and 
cognitive functions. Based on their strong association with disease, genetically 
and pathologically, it is not surprising that there has been a focus towards 
developing therapies against the aggregated structures. Unfortunately, current 
therapies have but mild benefit. With this in mind we will focus on the 
relationship of synaptic plasticity with Aβ and tau protein and their role as 
potential targets for the development of therapeutic drugs. Finally, we will 
provide perspectives in developing a multifactorial strategy for AD treatment.