Journal Article

DZNE-2025-01188

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png A systematic comparison of ATN biomarkers for monitoring longitudinal cognitive changes in Alzheimer's disease

Biel, D. ; Steward, A. ; Dewenter, A. ; Dehsarvi, A. ; Zhu, Z. ; Roemer-Cassiano, S. N. ; Frontzkowski, L. ; Hirsch, F. ; Palleis, C.DZNE* ; Höglinger, G.DZNE* ; Brendel, M.DZNE* ; Franzmeier, N.

2025
Wiley Hoboken, NJ

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Please use a persistent id in citations: doi:10.1002/alz.70783

Abstract: INTRODUCTIONWith anti-amyloid beta (Aβ) therapies approved for Alzheimer's disease (AD), surrogate biomarkers are needed to monitor clinical treatment efficacy. Therefore, we systematically compared longitudinal changes in A/T/N biomarkers (amyloid-positron emission tomography [PET], tau-PET, plasma phosphorylated tau at threonine 217 [p-tau217], and magnetic resonance imaging) for tracking cognitive changes.METHODSWe analyzed longitudinal biomarker and cognitive change rates from the Alzheimer's Disease Neuroimaging Initiative (N = 141) and Anti-Amyloid Treatment in Asymptomatic Alzheimer's (A4) and Longitudinal Evaluation of Amyloid Risk and Neurodegeneration (LEARN) (N = 151), estimated using linear mixed models. Using linear models, we tested biomarker changes as predictors of cognitive changes, comparing predictive strengths across biomarkers using bootstrapping.RESULTSTau-PET, plasma p-tau217, and cortical thickness changes accurately tracked change rates in Mini-Mental State Examination, Alzheimer's Disease Assessment Scale-Cognitive Subscale 13-item version, Clinical Dementia Rating-Sum of Boxes, and Preclinial Alzheimer Cognitive Composite scores. In contrast, amyloid-PET change rates were not linked to cognitive changes.DISCUSSIONPlasma p-tau217 offers a cost-effective AD-specific alternative to tau-PET and could potentially be implemented for monitoring cognitive changes in AD trials, while amyloid-PET lacks utility. Cortical thickness changes accurately track cognitive changes but may be confounded by pseudo-atrophy in anti-Aβ treatments.

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Contributing Institute(s):

1. Clinical Research (Munich) (Clinical Research (Munich))
2. Molecular Neurodegeneration (AG Haass)

Research Program(s):

1. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)
2. 352 - Disease Mechanisms (POF4-352) (POF4-352)

Appears in the scientific report 2025

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Database coverage:
; ; ; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; DEAL Wiley ; Essential Science Indicators ; IF >= 10 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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