%0 Journal Article
%T Results from the long-term extension of PRIME: A randomized Phase 1b trial of aducanumab.
%A Chen T
%A O'Gorman J
%A Castrillo-Viguera C
%A Rajagovindan R
%A Curiale GG
%A Tian Y
%A Patel D
%A von Rosenstiel P
%A von Hehn C
%A Salloway S
%A Hock C
%A Nitsch RM
%A Haeberlein SB
%A Sandrock A
%A Singhal P
%J Alzheimers Dement
%V 20
%N 5
%D 2024 05 3
%M 38567735
%F 16.655
%R 10.1002/alz.13755
%X Aducanumab selectively targets aggregated forms of amyloid beta (Aβ), a neuropathological hallmark of Alzheimer's disease (AD).<BR>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.<BR>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.<BR>The safety profile of aducanumab remained unchanged in the LTE of PRIME. Amyloid plaque levels continued to decrease in participants treated with aducanumab.<BR>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.