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Working memory gating in obesity is moderated by striatal dopaminergic gene variants

MPG-Autoren
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Herzog,  Nadine       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
International Max Planck Research School NeuroCom, Leipzig, Germany;

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Hartmann,  Hendrik       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Collaborative Research Center Obesity Mechanisms, Institute of Biochemistry, University of Leipzig, Germany;
Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Finland;

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Janssen,  Lieneke       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Institute of Psychology, Otto von Guericke University Magdeburg, Germany;

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Waltmann,  Maria       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Department of Child and Adolescent Psychiatry, Psychotherapy and Psychosomatics, University Hospital Würzburg, Germany;

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Villringer,  Arno       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Horstmann,  Annette       
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Collaborative Research Center Obesity Mechanisms, Institute of Biochemistry, University of Leipzig, Germany;
Department of Psychology and Logopedics, Faculty of Medicine, University of Helsinki, Finland;

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Herzog_2024.pdf
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Herzog_2024_Suppl.xlsx
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Zitation

Herzog, N., Hartmann, H., Janssen, L., Kanyamibwa, A., Waltmann, M., Kovacs, P., et al. (2024). Working memory gating in obesity is moderated by striatal dopaminergic gene variants. eLife, 13: RP93369. doi:10.7554/eLife.93369.


Zitierlink: https://hdl.handle.net/21.11116/0000-000D-E80F-E
Zusammenfassung
Everyday life requires an adaptive balance between distraction-resistant maintenance of information and the flexibility to update this information when needed. These opposing mechanisms are proposed to be balanced through a working memory gating mechanism. Prior research indicates that obesity may elevate the risk of working memory deficits, yet the underlying mechanisms remain elusive. Dopaminergic alterations have emerged as a potential mediator. However, current models suggest these alterations should only shift the balance in working memory tasks, not produce overall deficits. The empirical support for this notion is currently lacking, however. To address this gap, we pooled data from three studies (N = 320) where participants performed a working memory gating task. Higher BMI was associated with overall poorer working memory, irrespective of whether there was a need to maintain or update information. However, when participants, in addition to BMI level, were categorized based on certain putative dopamine-signaling characteristics (single-nucleotide polymorphisms [SNPs]; specifically, Taq1A and DARPP-32), distinct working memory gating effects emerged. These SNPs, primarily associated with striatal dopamine transmission, appear to be linked with differences in updating, specifically, among high-BMI individuals. Moreover, blood amino acid ratio, which indicates central dopamine synthesis capacity, combined with BMI shifted the balance between distractor-resistant maintenance and updating. These findings suggest that both dopamine-dependent and dopamine-independent cognitive effects exist in obesity. Understanding these effects is crucial if we aim to modify maladaptive cognitive profiles in individuals with obesity.