A renewed vision for Amyloid beta and tau in Alzheimer s disease pathophysiology

Abstract

The aim of this thesis was to study the pathogenetic mechanisms underlying Alzheimer s disease (AD), a neurodegenerative disorder affecting the elderly and characterized by memory loss, personality changes and cognitive dysfunction leading to dementia. I will discuss the main projects in which I participated aimed at understanding the role of the main molecular interactors involved in AD pathogenesis, i.e. Amyloid-beta peptide and tau protein, on hippocampal synaptic plasticity and memory in animal models. After reviewing the pathophysiological models that have been developed so far, our general purpose was to study novel aspects of Amyloid-beta peptide and tau involvement in physiological and pathological conditions to give a different interpretation of the disease.