[5][6] It is a monoclonal antibody[6][5] that targets aggregated forms (plaque)[7][8] of amyloid beta (Aβ) found in the brains of people with Alzheimer's disease to reduce its buildup.
[17] In November 2020, a panel of outside experts for the FDA concluded that a pivotal study of aducanumab failed to show strong evidence that the medication worked, citing questionable efficacy and multiple red flags found with the data analysis.
[6][20] The Office of Inspector General, US Department of Health and Human Services was asked to investigate interaction between the drug company and the FDA prior to the medication's approval.
[32] A 2023 review found that "Anti-Aβ drugs have relatively low efficacy in preventing cognitive decline, and they reduce pathological productions with acceptable safety.
"[2] In a 2023 commentary, the authors express concern that the results of the trials, which are based on scoring by patients and their caregivers, of these drugs could be confounded by unblinding produced by adverse effects.
[40] A 2024 study suggests that the cognitive benefits of monoclonal antibody treatments for Alzheimer’s disease may result from increases in Aβ42 levels, rather than solely from the removal of amyloid plaques.
[39] There are two categories of ARIA, based on signal changes believed to be associated with vasogenic edema (ARIA-E) and microhemorrhages (ARIA-H).
Brain volume loss is a symptom of Alzheimer's disease and is accelerated by anti-amyloid drugs developed to treat it.
One meta-analysis found that people with mild cognitive impairment treated with anti-amyloid drugs would reach the brain volume associated with full Alzheimer's disease eight months earlier than those who received no such treatment.