Alzheimer Disease (AD) is a common neurodegenerative disorder with an ever increasing impact in modern medicine, whose onset can be dated as early as 50 years of age. Numerous studies were performed to discover the biological underpinnings of this disease. Even though, it was demonstrated that AD has a genetic component, the genes and biological processes behind it, excluding some cases (5% of all cases) related to 3 genes (namely PSEN1, PSEN2, APP), remain largely unknown. Indeed, a lot of data has accumulated through the recent years evidencing the multifactorial nature of this disease. Nevertheless, a lot of data is accumulating focused on the pathways interacting with ?-Amyloid and Tau, the histopathological hallmarks of AD. The focus of this presentation will be the interaction of such pathways and how they interact with these anomalous proteins, causing AD onset and symptomatologic progression. Further, we will try to evidence possible central mechanisms toward which all these pathway converge