We introduce and study a new model for the progression of Alzheimer’s disease (AD) incorporating the interactions of A β -monomers, oligomers, microglial cells and interleukins with neurons through different mechanisms such as protein polymerization, inflammation processes and neural stress reactions. To understand the complete interactions between these elements, we study a spatially homogeneous simplified model that allows us to determine the effect of key parameters such as degradation rates in the asymptotic behaviour of the system and the stability of equilibrium. We observe that inflammation appears to be a crucial factor in the initiation and progression of AD through a phenomenon of hysteresis with respect to the oligomer degradation rate d . This means that depending on the advanced state of the disease (given by the value of the A β -monomer degradation rate d : large value for an early stage and low value for an advanced stage) there exists a critical threshold of initial concentration of interleukins that determines if the disease persists or not in the long term. These results give perspectives on possible anti-inflammatory treatments that could be applied to mitigate the progression of AD. We also present numerical simulations that allow us to observe the effect of initial inflammation and monomer concentration in our model.