PDF(Pubmed)
Abstract：
Aducanumab selectively targets aggregated forms of amyloid beta (Aβ), a neuropathological hallmark of Alzheimer\'s disease (AD).
PRIME was a Phase 1b, double-blind, randomized clinical trial of aducanumab. During the 12-month placebo-controlled period, participants with prodromal AD or mild AD dementia were randomized to receive aducanumab or placebo. At week 56, participants could enroll in a long-term extension (LTE), in which all participants received aducanumab. The primary endpoint was safety and tolerability.
Amyloid-related imaging abnormalities-edema (ARIA-E) were the most common adverse event. Dose titration was associated with a decrease in the incidence of ARIA-E. Over 48 months, aducanumab decreased brain amyloid levels in a dose- and time-dependent manner. Exploratory endpoints suggested a continued benefit in the reduction of clinical decline over 48 months.
The safety profile of aducanumab remained unchanged in the LTE of PRIME. Amyloid plaque levels continued to decrease in participants treated with aducanumab.
PRIME was a Phase 1b, double-blind, randomized clinical trial of aducanumab. We report cumulative safety and 48-month efficacy results from PRIME. Amyloid-related imaging abnormalities-edema (ARIA-E) were the most common adverse event (AE); 61% of participants with ARIA-E were asymptomatic. Dose titration was associated with a decrease in the incidence of ARIA-E. Aducanumab decreased levels of amyloid beta (Aβ) in a dose- and time-dependent manner.
PRIME was a Phase 1b, double-blind, randomized clinical trial of aducanumab. During the 12-month placebo-controlled period, participants with prodromal AD or mild AD dementia were randomized to receive aducanumab or placebo. At week 56, participants could enroll in a long-term extension (LTE), in which all participants received aducanumab. The primary endpoint was safety and tolerability.
Amyloid-related imaging abnormalities-edema (ARIA-E) were the most common adverse event. Dose titration was associated with a decrease in the incidence of ARIA-E. Over 48 months, aducanumab decreased brain amyloid levels in a dose- and time-dependent manner. Exploratory endpoints suggested a continued benefit in the reduction of clinical decline over 48 months.
The safety profile of aducanumab remained unchanged in the LTE of PRIME. Amyloid plaque levels continued to decrease in participants treated with aducanumab.
PRIME was a Phase 1b, double-blind, randomized clinical trial of aducanumab. We report cumulative safety and 48-month efficacy results from PRIME. Amyloid-related imaging abnormalities-edema (ARIA-E) were the most common adverse event (AE); 61% of participants with ARIA-E were asymptomatic. Dose titration was associated with a decrease in the incidence of ARIA-E. Aducanumab decreased levels of amyloid beta (Aβ) in a dose- and time-dependent manner.
摘要：
背景：Aducanumab选择性地靶向β淀粉样蛋白（Aβ）的聚集形式，阿尔茨海默病（AD）的神经病理学标志。
方法：PRIME是1b阶段，双盲,aducanumab的随机临床试验。在12个月的安慰剂对照期间，患有前驱AD或轻度AD痴呆的参与者被随机分配接受阿杜卡尼单抗或安慰剂治疗.在第56周，参与者可以注册长期扩展（LTE），所有参与者均接受了阿杜卡尼单抗治疗.主要终点是安全性和耐受性。
结果：淀粉样蛋白相关影像学异常-水肿（ARIA-E）是最常见的不良事件。剂量滴定与ARIA-E发生率的降低有关。超过48个月,aducanumab以剂量和时间依赖性方式降低脑淀粉样蛋白水平.探索性终点表明在48个月内临床下降的减少持续受益。
结论：在PRIME的LTE中，aducanumab的安全性保持不变。淀粉样蛋白斑块水平在接受aducanumab治疗的参与者中持续下降。
结论：PRIME是1b阶段，双盲,aducanumab的随机临床试验。我们报告了PRIME的累积安全性和48个月疗效结果。淀粉样蛋白相关的影像学异常-水肿（ARIA-E）是最常见的不良事件（AE）；61％的ARIA-E参与者无症状。剂量滴定与ARIA-E发生率的降低有关。Aducanumab以剂量和时间依赖性方式降低淀粉样β（Aβ）的水平。
方法：PRIME是1b阶段，双盲,aducanumab的随机临床试验。在12个月的安慰剂对照期间，患有前驱AD或轻度AD痴呆的参与者被随机分配接受阿杜卡尼单抗或安慰剂治疗.在第56周，参与者可以注册长期扩展（LTE），所有参与者均接受了阿杜卡尼单抗治疗.主要终点是安全性和耐受性。
结果：淀粉样蛋白相关影像学异常-水肿（ARIA-E）是最常见的不良事件。剂量滴定与ARIA-E发生率的降低有关。超过48个月,aducanumab以剂量和时间依赖性方式降低脑淀粉样蛋白水平.探索性终点表明在48个月内临床下降的减少持续受益。
结论：在PRIME的LTE中，aducanumab的安全性保持不变。淀粉样蛋白斑块水平在接受aducanumab治疗的参与者中持续下降。
结论：PRIME是1b阶段，双盲,aducanumab的随机临床试验。我们报告了PRIME的累积安全性和48个月疗效结果。淀粉样蛋白相关的影像学异常-水肿（ARIA-E）是最常见的不良事件（AE）；61％的ARIA-E参与者无症状。剂量滴定与ARIA-E发生率的降低有关。Aducanumab以剂量和时间依赖性方式降低淀粉样β（Aβ）的水平。
