Abstract
This article focused on discussing two monoclonal antibodies (mAbs), lecanemab and aducanumab, which target at amyloid-beta protofibrils and fibrils as amyloid-beta plaques are considered as the key pathogenesis of Alzheimer’s disease (AD). Detailed mechanism of AD including the formation of amyloid-beta plaques and tau protein was explained, as well as the efficacy, benefits and limitations of these two mAbs are discussed. Current studies shown that lecanemab and aducanumab have efficacy on reducing amyloid-beta plaques in AD patients. There are limitations to the usage of both lecanemab and aducanumab, such as the appearance of amyloid-relating imaging abnormalities (ARIA). However, findings suggested that less ARIA occurred in the administration of lecanemab, and to the most harmful kind of amyloid protein, lecanemab binds more tightly compared to aducanumab. Therefore, safety assessment of these two mAbs should also be considered. This article only focused on lecanemab and aducanumab, donanemab which was approved recently is not mentioned. It is worth pointing out that the appearance of lecanemab and aducanumab had revolutionized the treatment for AD, as this improve the life quality of AD patients. More effective mAbs and other treatments are still under investigations in order to lower the incidence, and provide more hope for curing AD.
Published Version
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