REAL-WORLD IMPACT OF ANTI-AMYLOID THERAPY IN ALZHEIMER’S DISEASE: AN INTEGRATED ANALYSIS OF 100% MEDICARE FFS CLAIMS LINKED WITH LABORATORY, ELECTRONIC MEDICAL RECORDS, AND PATIENT-REPORTED OUTCOMES MEASURES
Author(s)
Onur Baser, MA, MS, PhD1, Precious Nchekwube, MPH2, Nehir Yapar, BS2, Jialu He, MPH2;
1City University of New York (CUNY), Graduate School of Public Health, New York, NY, USA, 2Columbia Data Analytics, New York, NY, USA
1City University of New York (CUNY), Graduate School of Public Health, New York, NY, USA, 2Columbia Data Analytics, New York, NY, USA
OBJECTIVES: We evaluated the real-world impact of anti-amyloid treatment vs no treatment among Medicare fee-for-service beneficiaries diagnosed with Alzheimer’s disease (AD) using linked 100% CMS Medicare, laboratory, electronic medical records (EMR), and patient-reported outcome (PRO) measures, focusing on cognition, quality-of-life (QoL), and AD biomarkers.
METHODS: This retrospective analysis (2021-2024) used Columbia Data Analytics’ Medicare-Enhanced Lab & Demographics (MELDTM) dataset from beneficiaries aged ≥65 years diagnosed with AD, linked deterministically with laboratory, EMR, and dementia-specific PROs. From ~2.0M beneficiaries diagnosed with AD, ~120,000 had continuous enrollment and ≥1 linked EMR and PRO record. Of those, ~30,000 received anti-amyloid therapy (treatment group); ~90,000 did not (non-treatment group) (index date=first AD diagnosis/anti-amyloid claim; follow-up=24 months). Assessments: Cognition (Mini-Mental State Examination [MMSE], Montreal Cognitive Assessment [MoCA]; QoL (Dementia QoL Measure [DEMQoL], QoL-AD); biomarkers (cerebrospinal fluid [CSF]/plasma Aβ42, Aβ40, Aβ42/40 ratio, total tau, phosphorylated tau). Multivariable regression and inverse probability of treatment weighting adjusted for demographics, comorbidities, cognitive scores, and biomarkers.
RESULTS: Baseline mean MMSE scores: 22 (treatment), 21 (non-treatment); mean MoCA scores: 18 and 17, respectively. Treated patients showed an adjusted 2-year mean MMSE decline of 2 vs 4 points (non-treatment); adjusted mean MoCA scores declined 3 vs 6 points, corresponding to a 40-50% relative slowing cognitive decline. Baseline DEMQoL (scale=0-100): ~62 in both groups, declined by 3 (treatment) vs 7 points (non-treatment); QoL-AD (scale=13-52) decreased from ~40 to 38, vs 40 to 34, respectively. Anti-amyloid therapy showed greater improvement in Aβ42/40 ratio (mean increase=0.03 vs 0.01), and greater reductions in total tau (−10% vs −3%) and phosphorylated tau (−18% vs −5%) vs non-treatment.
CONCLUSIONS: Anti-amyloid use was associated with slower cognitive decline, smaller QoL decline, and favorable changes in AD biomarkers vs non-treatment, supporting the benefit of treatment in routine practice and demonstrating the value of integrated Medicare-EMR-PRO data for AD-related health technology assessments.
METHODS: This retrospective analysis (2021-2024) used Columbia Data Analytics’ Medicare-Enhanced Lab & Demographics (MELDTM) dataset from beneficiaries aged ≥65 years diagnosed with AD, linked deterministically with laboratory, EMR, and dementia-specific PROs. From ~2.0M beneficiaries diagnosed with AD, ~120,000 had continuous enrollment and ≥1 linked EMR and PRO record. Of those, ~30,000 received anti-amyloid therapy (treatment group); ~90,000 did not (non-treatment group) (index date=first AD diagnosis/anti-amyloid claim; follow-up=24 months). Assessments: Cognition (Mini-Mental State Examination [MMSE], Montreal Cognitive Assessment [MoCA]; QoL (Dementia QoL Measure [DEMQoL], QoL-AD); biomarkers (cerebrospinal fluid [CSF]/plasma Aβ42, Aβ40, Aβ42/40 ratio, total tau, phosphorylated tau). Multivariable regression and inverse probability of treatment weighting adjusted for demographics, comorbidities, cognitive scores, and biomarkers.
RESULTS: Baseline mean MMSE scores: 22 (treatment), 21 (non-treatment); mean MoCA scores: 18 and 17, respectively. Treated patients showed an adjusted 2-year mean MMSE decline of 2 vs 4 points (non-treatment); adjusted mean MoCA scores declined 3 vs 6 points, corresponding to a 40-50% relative slowing cognitive decline. Baseline DEMQoL (scale=0-100): ~62 in both groups, declined by 3 (treatment) vs 7 points (non-treatment); QoL-AD (scale=13-52) decreased from ~40 to 38, vs 40 to 34, respectively. Anti-amyloid therapy showed greater improvement in Aβ42/40 ratio (mean increase=0.03 vs 0.01), and greater reductions in total tau (−10% vs −3%) and phosphorylated tau (−18% vs −5%) vs non-treatment.
CONCLUSIONS: Anti-amyloid use was associated with slower cognitive decline, smaller QoL decline, and favorable changes in AD biomarkers vs non-treatment, supporting the benefit of treatment in routine practice and demonstrating the value of integrated Medicare-EMR-PRO data for AD-related health technology assessments.
Conference/Value in Health Info
2026-05, ISPOR 2026, Philadelphia, PA, USA
Value in Health, Volume 29, Issue S6
Code
CO21
Topic
Clinical Outcomes
Disease
SDC: Neurological Disorders