Moderator of 1 Session
Session Description:
This symposium will introduce the need for new treatments for Alzheimer’s disease and Parkinson’s disease that go beyond symptomatic control and potentially treat the underlying causes of each disease. During this session, the pathophysiology of Alzheimer’s disease will be examined and drug targets other than amyloid and tau considered, including key data published on these targets to date. There will also be a presentation on neuroinflammation as an aspect of neurodegenerative diseases and a potential target for the treatment of both Alzheimer’s disease and Parkinson’s disease. Finally current treatments for Parkinson’s disease will be discussed briefly, as well as treatments currently being investigated in clinical trials, to provide a perspective on how the treatment landscape may change from symptomatic control to treatment in the future. These topics will be discussed by the expert faculty, who will also address any questions from attendees.
Presenter of 4 Presentations
Panel discussion: What does the future hold for people with AD and PD? Summary and meeting close
Summary and meeting close
Welcome and introduction
KEY TRIAL DESIGN ASPECTS AND CLINICAL OUTCOMES OF THE LECANEMAB PHASE 2 TRIAL AND OPEN-LABEL EXTENSION IN EARLY ALZHEIMER’S DISEASE
Abstract
Aims
Lecanemab is a humanized IgG1 monoclonal antibody that selectively targets soluble aggregated Aβ species. Key design features and latest results will be presented from a large, double-blind, placebo-controlled, randomized 18-month phase 2 proof-of-concept Core study (Study 201) with a Bayesian design and an open-label extension (OLE) recently conducted in early Alzheimer’s disease (AD).
Methods
In this presentation, the design and latest results from the lecanemab Study 201 Core, in which patients were randomized to five dose regimens or placebo will be reviewed. The latest data from the open-label extension (OLE) of Study 201, which was initiated to allow patients to receive open-label lecanemab 10mg/kg-biweekly for up to 24 months will also be reviewed.
Results
Lecanemab treatment can be initiated without titration and results in rapid and thorough amyloid reduction correlating with clinical benefit. Amyloid reduction achieved within 3 months and clinical efficacy within 6 months of treatment. Benefit in early AD patients is maintained after treatment discontinuation, suggesting potential disease modifying effects. ARIA-E and symptomatic ARIA rates were low in the Core and OLE. These data are supportive of important therapeutic effects and are supported by changes in key biomarkers as discussed by the next speaker. These findings will be further evaluated in the phase 3 Clarity AD trial which is ongoing.
Conclusions
The findings from Study 201 Core and OLE suggest that lecanemab 10mg/kg biweekly can be initiated to elicit rapid reduction of brain amyloid at the onset of treatment with relatively low incidence and severity of ARIA-E.