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Journal Article

Resting-State Network Alterations Differ between Alzheimer’s Disease Atrophy Subtypes

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Scheffler,  K
Max Planck Institute for Biological Cybernetics, Max Planck Society;
Department High-Field Magnetic Resonance, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Citation

Rauchmann, B.-S., Ersoezlue, E., Stoecklein, S., Keeser, D., Brosseron, F., Buerger, K., et al. (2021). Resting-State Network Alterations Differ between Alzheimer’s Disease Atrophy Subtypes. Cerebral Cortex, 31(11), 4901-4915. doi:10.1093/cercor/bhab130.


Cite as: http://hdl.handle.net/21.11116/0000-0009-F32A-6
Abstract
everal Alzheimer’s disease (AD) atrophy subtypes were identified, but their brain network properties are unclear. We analyzed data from two independent datasets, including 166 participants (103 AD/63 controls) from the DZNE-longitudinal cognitive impairment and dementia study and 151 participants (121 AD/30 controls) from the AD neuroimaging initiative cohorts, aiming to identify differences between AD atrophy subtypes in resting-state functional magnetic resonance imaging intra-network connectivity (INC) and global and nodal network properties. Using a data-driven clustering approach, we identified four AD atrophy subtypes with differences in functional connectivity, accompanied by clinical and biomarker alterations, including a medio-temporal-predominant (S-MT), a limbic-predominant (S-L), a diffuse (S-D), and a mild-atrophy (S-MA) subtype. S-MT and S-D showed INC reduction in the default mode, dorsal attention, visual and limbic network, and a pronounced reduction of “global efficiency” and decrease of the “clustering coefficient” in parietal and temporal lobes. Despite severe atrophy in limbic areas, the S-L exhibited only marginal global network but substantial nodal network failure. S-MA, in contrast, showed limited impairment in clinical and cognitive scores but pronounced global network failure. Our results contribute toward a better understanding of heterogeneity in AD with the detection of distinct differences in functional connectivity networks accompanied by CSF biomarker and cognitive differences in AD subtypes.