The aggregation and accumulation of oligomers of misfolded A \(\beta\) -amyloids in the human brain is one of the possible causes for the onset of the Alzheimer’s disease in the early stage. We introduce and study a new ODE model for the evolution of Alzheimer’s disease based on the interaction between monomers, proto-oligomers, and oligomers of A \(\beta\) amyloid protein in a small portion of the human brain, based upon biochemical processes such as polymerization, depolymerization, fragmentation and concatenation. We further introduce the possibility of controlling the evolution of the system via a treatment that targets the monomers and/or the oligomers. We observe that a combined optimal treatment on both monomers and oligomers induces a substantial decrease of the oligomer concentration at the final stage. A single treatment on oligomers performs better than a single treatment on monomers. These results shed a light on the effectiveness of immunotherapy using anti-A \(\beta\) antibodies, targeting monomers or oligomers. Several numerical simulations show how the oligomer concentration evolves without treatment, with single monomer/oligomer treatment, or with a combined treatment.
