Use of lecanemab and donanemab in the Canadian healthcare system: Evidence, challenges, and areas for future research
Eric E. Smith, Natalie A. Phillips, Howard Feldman, Michael Borrie, Aravind Ganesh, Alexandre Henri‐Bhargava, Philippe Desmarais, Andrew Frank, AmanPreet Badhwar, Laura Barlow, Robert Bartha, Sarah Best, Jennifer Bethell, Jaspreet Bhangu, Sandra E. Black, Christian Bocti, Susan E. Bronskill, Amer M. Burhan, Frédéric Calon, Richard Camicioli, Barry Campbell, D. Louis Collins, Mahsa Dadar, Mari L. DeMarco, Simon Ducharme, Simon Duchesne, Gillian Einstein, John D. Fisk, Jodie R. Gawryluk, Linda Grossman, Zahinoor Ismail, Inbal Itzhak, Manish Joshi, Arthur Harrison, Edeltraut Kröger, Sanjeev Kumar, Robert Laforce, Krista L. Lanctôt, Malena Lau, Linda Lee, Mario Masellis, Fadi Massoud, Sara Mitchell, Manuel Montero‐Odasso, Karen Myers Barnett, Haakon B. Nygaard, Stephen Pasternak, Jody Peters, M. Natasha Rajah, Julie M. Robillard, K. Rockwood, Pedro Rosa‐Neto, Dallas Seitz, Jean‐Paul Soucy, Shanna Trenaman, Cheryl L. Wellington, Aicha Zadem, Howard Chertkow
Abstract
Lecanemab and donanemab are monoclonal antibody therapies that remove amyloid-beta from the brain. They are the first therapies that alter a fundamental mechanism, amyloid-beta deposition, in Alzheimer disease (AD). To inform Canadian decisions on approval and use of these drugs, the Canadian Consortium on Neurodegeneration in Aging commissioned Work Groups to review evidence on the efficacy and safety of these new therapies, as well as their projected impacts on Canadian dementia systems of care. We included persons with lived experience with Alzheimer disease in the discussion about the benefits and harms. Our review of the trial publications found high quality evidence of statistically significant group differences, but also recognized that there are mixed views on the clinical relevance of the observed differences and the value of therapy for individual patients. The drugs are intended for persons with early AD, at a stage of mild cognitive impairment or mild dementia. If patients are treated, then confirmation of AD by positron emission tomography or cerebrospinal fluid analysis and monitoring for risk of amyloid-related imaging abnormalities was recommended, as done in the clinical trials, although it would strain Canadian resource capacity. More data are needed to determine the size of the potentially eligible treatment population in Canada.