The main pathological features of Alzheimer's disease (AD) include the cytotoxic extracellular accumulation of the amyloid beta (A beta) plaques and intracellular neurofibrillary tangles. The A beta plaques are responsible for cholinergic dysfunction and dementia in AD patients. Immunoglobulin G (IgG) and A beta form an immune complex that activates neuroglia, clearing A beta from the brain. Various A beta-based therapeutic strategies have been proposed to reduce A beta production, inhibit A beta aggregation, and increase A beta clearance. New medicines, such as aducanumab and donanemab, which are human IgG1 monoclonal antibodies, reduce cognitive impairment in patients with AD by decreasing the amount of A beta plaques. Despite the considerable advantages of these agents, some disadvantages have also been reported, including A beta-related imaging abnormalities, anaphylaxis, high cost, and contradictory results. Moreover, donanemab has delivered contradictory outcomes in improving recognition and performance in AD. However, although not fully proven yet, fewer side effects are reported for donanemab compared to aducanumab. Therefore, this review aims to explore the research background, compare the mechanism of action, and understand the advantages and disadvantages of aducanumab and donanemab. As a result, these medicines with maximum effectiveness and safety, yet fewer side effects, could be