In a stunning reversal last October, pharma giant Biogen announced that its failed Phase 3 clinical trial of aducanemab in people with mild cognitive impairment or mild Alzheimer’s disease didn’t actually fail. More details were released this month at the Clinical Trials in Alzheimer’s Disease conference in San Diego. LBDA’s Todd Graham, Executive Director, was there to hear the details.
Running two trials in parallel, EMERGE and ENGAGE, participants received varying doses of an antibody drug over 18 months that targets the build-up of amyloid in the brain. Over 3,000 participants with mild cognitive impairment due to Alzheimer’s disease (AD) or mild AD dementia were enrolled in these international studies.
Those in EMERGE were randomized to receive a placebo or a higher dose of aducanumab for 18 months; once all of the subjects’ data was compiled, cognitive assessments revealed those receiving the study drug had a 40% slower rate of cognitive decline over placebo. Participants in ENGAGE were given a lower dose of the study drug; while they showed no significant slowing of cognitive decline, a reduction of amyloid was evident via PET imaging and that in a subgroup of people who had received many more doses of aducanumab declined more slowly.
“Most people with Lewy body dementia (LBD) also have some changes of Alzheimer’s disease in the brain,” stated LBDA’s Todd Graham. “Research indicates people with LBD and co-existing Alzheimer’s disease may have a more aggressive progression. It is imperative that successful Alzheimer’s disease-modifying therapies also be studied in people with LBD.”
There are mixed opinions in the scientific community on whether these two trials provide enough evidence for regulatory approval for the marketing of aducanumab for Alzheimer’s disease. Biogen is moving forward with an application to the US Food and Drug Administration (FDA) for marketing approval.
Will the FDA approve their application or is more data needed to confirm the drug is both safe and effective? Only time will tell. Our fingers are crossed that this time allows for the consideration of additional study of this and other disease-modifying AD drugs in people with LBD.