New research indicates that donanemab, a drug approved in the United Kingdom for the treatment of Alzheimer’s disease, may slow disease progression for up to three years by effectively removing amyloid plaques from the brain. The findings offer renewed hope for a treatment that could extend patients’ cognitive function and independence over a longer timeframe than previously understood.
The study tracked more than 1,200 patients either treated with donanemab or switched to the drug after initially receiving a placebo. Brain imaging showed that toxic amyloid plaques—considered a hallmark of Alzheimer’s—remained undetectable approximately three years after the start of treatment. This contrasts with earlier data based on an 18-month trial, which demonstrated that donanemab reduced cognitive decline by 35 percent in eligible patients. The extended follow-up highlights sustained benefits beyond the initial treatment period, including a continued reduction in a tau protein associated with brain damage and cognitive impairment.
Donanemab, marketed as Kisunla, was licensed in the UK in 2024; however, it has not yet been approved for use on the National Health Service (NHS) due to concerns over cost-effectiveness. An appeal is currently underway in hopes of securing NHS availability. This new evidence that donanemab’s effects endure for multiple years may strengthen arguments regarding its value, particularly given that treatment consists of infusions that could become less frequent over time.
The trial results, presented at the Alzheimer’s Association International Conference in London, showed a clinically meaningful difference in cognitive function between treated patients and those who did not receive the drug. Patients on donanemab scored 0.6 points higher on the 18-point Clinical Dementia Rating Scale after 18 months, with the gap increasing to 1.2 points after three years. Notably, this benefit persisted even after regular infusions ceased, indicating ongoing advantages after clearance of amyloid plaques.
In addition to these clinical outcomes, the study found significant reductions in p-tau217, a blood biomarker for tau pathology, during early treatment stages. Researchers also noted progress in minimizing adverse effects such as brain bleeds, which have previously limited the tolerability of amyloid-targeting therapies.
Experts welcomed the findings as supporting the potential of amyloid-focused drugs to slow Alzheimer’s progression, especially when initiated early. Hilary Evans-Newton, chief executive of Alzheimer’s Research UK, emphasized the importance of these results in addressing ongoing scientific debates about the safety and efficacy of anti-amyloid strategies. Meanwhile, Dr. Nick Fox, director of the Dementia Research Centre at University College London, highlighted the value of treatments that could help patients maintain independence for longer periods, particularly given the slow development of Alzheimer’s over decades.
Researchers are now exploring whether cognitive benefits can be preserved with less frequent maintenance infusions after initial treatment completion. Meanwhile, trials for a next-generation drug, dontrinemab, are set to begin enrolling people at high risk of Alzheimer’s but without symptoms, aiming to prevent dementia before clinical decline occurs.
