TY - JOUR
T1 - Sample size estimates for biomarker-based outcome measures in clinical trials in autosomal dominant Alzheimer's disease
AU - Dominantly Inherited Alzheimer Network (DIAN)
AU - Cash, David M.
AU - Morgan, Katy E.
AU - O'Connor, Antoinette
AU - Veale, Thomas D.
AU - Malone, Ian B.
AU - Poole, Teresa
AU - Benzinger, Tammie Ls
AU - Gordon, Brian A.
AU - Ibanez, Laura
AU - Li, Yan
AU - Llibre-Guerra, Jorge J.
AU - McDade, Eric
AU - Wang, Guoqiao
AU - Chhatwal, Jasmeer P.
AU - Day, Gregory S.
AU - Huey, Edward
AU - Jucker, Mathias
AU - Levin, Johannes
AU - Niimi, Yoshiki
AU - Noble, James M.
AU - Roh, Jee Hoon
AU - Sánchez-Valle, Racquel
AU - Schofield, Peter R.
AU - Bateman, Randall J.
AU - Frost, Chris
AU - Fox, Nick C.
N1 - Publisher Copyright:
Copyright © 2025 The Author(s). Published by Elsevier Masson SAS.. All rights reserved.
PY - 2025/6/1
Y1 - 2025/6/1
N2 - INTRODUCTION: Alzheimer disease (AD)-modifying therapies are approved for treatment of early-symptomatic AD. Autosomal dominant AD (ADAD) provides a unique opportunity to test therapies in presymptomatic individuals. METHODS: Using data from the Dominantly Inherited Alzheimer Network (DIAN), sample sizes for clinical trials were estimated for various cognitive, imaging, and CSF outcomes. Sample sizes were computed for detecting a reduction of either absolute levels of AD-related pathology (amyloid, tau) or change over time in neurodegeneration (atrophy, hypometabolism, cognitive change). RESULTS: Biomarkers measuring amyloid and tau pathology had required sample sizes below 200 participants per arm (examples CSF Aβ42/40: 47[95 %CI 25,104], cortical PIB 49[28,99], CSF p-tau181 74[48,125]) for a four-year trial in presymptomatic individuals (CDR=0) to have 80 % power (5 % statistical significance) to detect a 25 % reduction in absolute levels of pathology, allowing 40 % dropout. For cognitive, MRI, and FDG, it was more appropriate to detect a 50 % reduction in rate of change. Sample sizes ranged from 250 to 900 (examples hippocampal volume: 338[131,2096], cognitive composite: 326[157,1074]). MRI, FDG and cognitive outcomes had lower sample sizes when including indivduals with mild impairment (CDR=0.5 and 1) as well as presymptomatic individuals (CDR=0). DISCUSSION: Despite the rarity of ADAD, presymptomatic clinical trials with feasible sample sizes given the number of cases appear possible.
AB - INTRODUCTION: Alzheimer disease (AD)-modifying therapies are approved for treatment of early-symptomatic AD. Autosomal dominant AD (ADAD) provides a unique opportunity to test therapies in presymptomatic individuals. METHODS: Using data from the Dominantly Inherited Alzheimer Network (DIAN), sample sizes for clinical trials were estimated for various cognitive, imaging, and CSF outcomes. Sample sizes were computed for detecting a reduction of either absolute levels of AD-related pathology (amyloid, tau) or change over time in neurodegeneration (atrophy, hypometabolism, cognitive change). RESULTS: Biomarkers measuring amyloid and tau pathology had required sample sizes below 200 participants per arm (examples CSF Aβ42/40: 47[95 %CI 25,104], cortical PIB 49[28,99], CSF p-tau181 74[48,125]) for a four-year trial in presymptomatic individuals (CDR=0) to have 80 % power (5 % statistical significance) to detect a 25 % reduction in absolute levels of pathology, allowing 40 % dropout. For cognitive, MRI, and FDG, it was more appropriate to detect a 50 % reduction in rate of change. Sample sizes ranged from 250 to 900 (examples hippocampal volume: 338[131,2096], cognitive composite: 326[157,1074]). MRI, FDG and cognitive outcomes had lower sample sizes when including indivduals with mild impairment (CDR=0.5 and 1) as well as presymptomatic individuals (CDR=0). DISCUSSION: Despite the rarity of ADAD, presymptomatic clinical trials with feasible sample sizes given the number of cases appear possible.
KW - Alzheimer's disease
KW - Autosomal dominant
KW - CSF
KW - Clinical trials
KW - Linear mixed effects models
KW - Longitudinal
KW - MRI
KW - PET
KW - Sample size
KW - ß-amyloid
UR - https://www.scopus.com/pages/publications/105010568774
U2 - 10.1016/j.tjpad.2025.100133
DO - 10.1016/j.tjpad.2025.100133
M3 - Article
C2 - 40118731
AN - SCOPUS:105010568774
SN - 2274-5807
VL - 12
SP - 100133
JO - The journal of prevention of Alzheimer's disease
JF - The journal of prevention of Alzheimer's disease
IS - 6
ER -