The aim of this paper is to clarify the pathology of Alzheimer's disease (AD), describe the mechanisms of its onset, and outline the proteins associated with the disease's pathology. It particularly focuses on the use of monoclonal antibodies in therapy of the disease, with an emphasis on ADUCANUMAB. The paper provides a detailed description of the methods of antibody production, their therapeutic basis, mechanisms of action, and effectiveness in treating Alzheimer's disease. Alzheimer's disease is a severe neurodegenerative condition that manifests through a range of subtle symptoms. Symptoms can vary widely, from short-term memory loss to hallucinations and delusions. Pathogenesis involves the accumulation of amyloid-β peptides (Aβ) in the brain and cytoskeletal changes caused by hyperphosphorylation of Tau proteins. Research is focused on understanding the mechanisms of disease onset, including genetic factors such as APP, PSEN1, PSEN2, and APOE-e4, and environmental influences. Methods include a review of the literature on the pathogenesis, symptoms, and treatment of Alzheimer's disease, as well as laboratory techniques for the production and testing of the effectiveness of monoclonal antibodies. Monoclonal antibodies, including ADUCANUMAB, have shown a reduction in amyloid plaques in the brain and improvement in cognitive functions in preclinical and clinical trials. ADUCANUMAB selectively binds to aggregated forms of Aβ, activating macrophages that degrade the plaques without significant side effects. Phase I, II, and III clinical trials demonstrate a reduction in Aβ plaques and slowing of cognitive decline, although not all clinically significant results have been achieved. Monoclonal antibodies represent a promising option for future treatment but require further research and clinical trials.