SEATTLE – An update from a phase 2 study – core and open-label extension – of lecanemab in Alzheimer's disease showed that the antibody reduced amyloid plaques within the first months after treatment initiation, and this effect was associated with improved clinical signs in as early as 6 months. The researchers identified two plasma biomarkers that correlate well with established amyloid PET standard uptake value ratio (SUVr) changes, potentially paving the way for monitoring lecanemab treatment effects. The researchers also found evidence that the plasma biomarker could be used to allow dose frequency reduction after initial reduction in amyloid plaques.
Lecanemab preferably targets aggregated species of amyloid called protofibrils, which is unique among anti-amyloid antibodies, and these are also among the most toxic manifestations of amyloid, according to Chad Swanson, PhD, who presented the study at the 2022 annual meeting of the American Academy of Neurology.
Are Amyloid Plaques a Key Driver of Alzheimer’s Disease?
The study could help answer the question of whether amyloid plaques drive the cognitive decline seen in Alzheimer's disease, in part because the antibody is so effective at what it was designed to do, according to Fernando Testai, MD, PhD, who comoderated the session where the study was presented. "The effect on amyloid content that they measured was persistent over a number of months.
