Abstract
INTRODUCTION
Aducanumab selectively targets aggregated forms of amyloid beta (Aβ), a neuropathological hallmark of Alzheimer’s disease (AD).
METHODS
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.
RESULTS
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.
DISCUSSION
The safety profile of aducanumab remained unchanged in the LTE of PRIME. Amyloid plaque levels continued to decrease in participants treated with aducanumab.
Highlights
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.
If you do not see content above, kindly GO TO SOURCE.
Not all publishers encode content in a way that enables republishing at Neuro.vip.
This post is Copyright: Tianle Chen,
John O’Gorman,
Carmen Castrillo‐Viguera,
Rajasimhan Rajagovindan,
Gioacchino G. Curiale,
Ying Tian,
Dakshaben Patel,
Philipp von Rosenstiel,
Christian von Hehn,
Stephen Salloway,
Christoph Hock,
Roger M. Nitsch,
Samantha Budd Haeberlein,
Alfred Sandrock,
Priya Singhal | April 3, 2024