International Alzheimer
International Alzheimer’s disease prevention trial in at-risk young adults begins
An international clinical trial aimed at preventing Alzheimer’s disease (AD) in young adults who are at risk of developing the neurodegenerative disorder has begun. Led by Washington University School of Medicine, the Primary Prevention Trial will enrol approximately 240 individuals from families that carry mutations in one of the three key genes associated with early-onset AD.
Participants will be as young as 18 years and have few or no detectable AD-related molecular changes in their brains.
AD is the most common form of dementia, affecting approximately seven million people in the US. Both genetic and non-genetic forms of the disease start with the amyloid beta protein slowly collecting in the brain two decades before the onset of memory and thinking problems.
The study is part of the Knight Family Dominantly Inherited Alzheimer Network-Trials Unit (Knight Family DIAN-TU) and will evaluate whether remternetug, an investigational antibody being developed by Eli Lilly, can remove amyloid beta from the brain or block it from accumulating in the first place.
Participants will recieve remternetug, administered via an injection under the skin, or placebo every three months for two years. At the end of the experimental period, those who carry a mutation will be eligible to receive Lilly’s drug for an additional four years as part of an open-label extension.
Lilly received regulatory approvals for another amyloid plaque-targeting AD drug, Kisunla (donanemab), last year, and Eisai/Biogen’s amyloid-targeting AD treatment Leqembi (lecanemab) also recently gained approvals.
Eric McDade, a professor of neurology and the trial’s principal investigator, said: “We have seen tremendous progress in the treatment of AD in the past few years. Two amyloid-targeting drugs were shown to slow symptoms of the disease and have now been approved by the Food and Drug Administration as treatments for people with mild cognitive impairment or mild dementia due to AD. This provides strong support for our hypothesis that intervening when amyloid beta plaques are at the very earliest stage, long before symptoms arise, could prevent symptoms from emerging in the first place.”
Mark Mintun, group vice president-neuroscience research and development at Lilly, added: “We are pleased to partner with the DIAN-TU team to evaluate whether remternetug can help slow or prevent the accumulation of amyloid plaque, a defining event in the early cascade of AD onset.”
