Kepp Kasper P, Sensi Stefano L, Johnsen Kasper B, Barrio Jorge R, Høilund-Carlsen Poul F, Neve Rachael L, Alavi Abass, Herrup Karl, Perry George, Robakis Nikolaos K, Vissel Bryce, Espay Alberto J
Department of Chemistry, Section of Biophysical and Biomedicinal Chemistry, Technical University of Denmark, Kongens Lyngby, Denmark.
Center for Advanced Studies and Technology - CAST, and Institute for Advanced Biotechnology (ITAB), University G. d'Annunzio of Chieti-Pescara, Italy.
J Alzheimers Dis. 2023;94(2):497-507. doi: 10.3233/JAD-230099.
After the CLARITY-AD clinical trial results of lecanemab were interpreted as positive, and supporting the amyloid hypothesis, the drug received accelerated Food and Drug Administration approval. However, we argue that benefits of lecanemab treatment are uncertain and may yield net harm for some patients, and that the data do not support the amyloid hypothesis. We note potential biases from inclusion, unblinding, dropouts, and other issues. Given substantial adverse effects and subgroup heterogeneity, we conclude that lecanemab's efficacy is not clinically meaningful, consistent with numerous analyses suggesting that amyloid-β and its derivatives are not the main causative agents of Alzheimer's disease dementia.
在lecanemab的CLARITY-AD临床试验结果被解读为阳性并支持淀粉样蛋白假说后,该药物获得了美国食品药品监督管理局的加速批准。然而,我们认为lecanemab治疗的益处尚不确定,可能会对一些患者产生净伤害,并且现有数据并不支持淀粉样蛋白假说。我们注意到纳入、揭盲、退出及其他问题可能带来的偏差。鉴于存在大量不良反应和亚组异质性,我们得出结论,lecanemab的疗效在临床上并无意义,这与众多分析结果一致,即淀粉样β蛋白及其衍生物并非阿尔茨海默病性痴呆的主要致病因素。