A2 Vertaisarvioitu katsausartikkeli tieteellisessä lehdessä

Longitudinal biomarker studies in human neuroimaging: capturing biological change of Alzheimer’s pathology




TekijätFischer, Larissa; Parker, Dana; Maboudian, Samira; Fonseca, Corrina; Tato-Fernández, Claudia; Annen, Lucie; Arunachalam, Prithvi; Bacci, Julia R.; Barboure, Michelle; Capelli, Serena; Karagianni, Stamatia; Collij, Lyduine E.; Edison, Paul; Fox, Nick C.; Franzmeier, Nicolai; Grothe, Michel J.; Jagust, William J.; Maass, Anne; Malpetti, Maura; Paterson, Ross W.; Sogorb-Esteve, Aitana; Schöll, Michael

KustantajaBioMed Central

Julkaisuvuosi2026

Lehti: Alzheimer's Research and Therapy

Artikkelin numero13

Vuosikerta18

eISSN1758-9193

DOIhttps://doi.org/10.1186/s13195-025-01920-6

Julkaisun avoimuus kirjaamishetkelläAvoimesti saatavilla

Julkaisukanavan avoimuus Kokonaan avoin julkaisukanava

Verkko-osoitehttps://doi.org/10.1186/s13195-025-01920-6

Rinnakkaistallenteen osoitehttps://research.utu.fi/converis/portal/detail/Publication/505810761

Rinnakkaistallenteen lisenssiCC BY

Rinnakkaistallennetun julkaisun versioKustantajan versio


Tiivistelmä

Despite extensive research, open questions about the biological underpinnings of Alzheimer’s disease (AD) remain. Neuroimaging biomarkers based on positron emission tomography (PET) and magnetic resonance imaging (MRI) offer in vivo insights into these complex biological changes and interactions. However, most evidence to date comes from cross-sectional studies, limiting our understanding of disease progression. Longitudinal studies enable the investigation of biological changes within individuals, revealing how pathology evolves over time. With this review, we provide an overview of how longitudinal imaging biomarker studies have advanced the field and how they can contribute to future research. We highlight longitudinal biomarker studies that have provided critical insights into disease trajectories, staging, and individual variability. We further assess longitudinal multimodal studies which have elucidated interactions between AD-specific pathology, amyloid-β and tau, and broader biological changes like neurodegeneration, neuronal dysfunction, vascular disease, and inflammation. Further, we discuss associations of brain changes with symptomatology and clinical outcomes and conclude with challenges and future directions.


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This is an electronic reprint of the original article.
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Open access funding provided by University of Gothenburg. This research did not receive any specific grant from funding agencies in the public, commercial or not-for-profit sectors. Open access funding was provided by the University of Gothenburg.


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