Long-Term Health Outcomes of Lecanemab in Patients with Early Alzheimer's Disease Using Simulation Modeling

Neurol Ther. 2022 Jun;11(2):863-880. doi: 10.1007/s40120-022-00350-y. Epub 2022 Apr 25.


Introduction: Alzheimer's disease (AD) is a progressive, neurodegenerative disease and is the most common cause of dementia. Lecanemab is a humanized monoclonal antibody targeting amyloid protofibrils for the treatment of early AD. In the phase II BAN2401-G000-201 trial (NCT01767311), lecanemab reduced amyloid accumulated in the brain and slowed progression on key global and cognitive scales evaluating efficacy after 18 months of treatment.

Methods: A disease simulation model was used to predict the long-term clinical outcomes of lecanemab for patients with early AD [i.e., mild cognitive impairment (MCI) due to AD and mild AD dementia] on the basis of BAN2401-G000-201 trial data and published literature. The model captures the pathophysiology and management of AD, with a focus on simulating the effects of disease modification and early intervention on disease progression. The model compares lecanemab in addition to standard of care (SoC) versus SoC alone.

Results: Lecanemab treatment was estimated to slow the rate of disease progression, resulting in an extended duration of MCI due to AD and mild AD dementia and shortened duration in moderate and severe AD dementia. The mean time to mild, moderate, and severe AD dementia was longer for patients in the lecanemab + SoC group than for patients in the SoC group by 2.51, 3.13, and 2.34 years, respectively. On base-case analysis, lecanemab was associated with 0.73 incremental life years (LY) and 0.75 incremental quality-adjusted LYs (QALY), and the caregiver QALYs lost was reduced by 0.03 years. The model also predicted a lower lifetime probability of admission to institutional care in lecanemab + SoC versus SoC group (25% versus 31%).

Conclusion: The model results demonstrate the potential clinical value of lecanemab for patients with early AD and how it can slow the rate of disease progression and reduce the lifetime probability for institutionalized care.

Keywords: Alzheimer’s disease; Amyloid plaques; Disease-modifying therapy; Institutionalization; Lecanemab; Progression; Simulation.