Evidence map›Paper›PMID 42168586›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2026

Nutritional state-dependent changes in subcortical limbic structures in anorexia nervosa are linked to leptin, ghrelin, and neurofilament light.

Marie-Louis Wronski, Klaas Bahnsen, Fabio Bernardoni, Maria Seidel, Arne Doose, Inger Hellerhoff, Milena Schimack, Jonas L Steinhäuser, Giulia Lombardo, Johanna L Keeler and 7 more

Abstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Marie-Louis WronskiTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.
Klaas BahnsenTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.ORCID http://orcid.org/0000-0002-5413-0359
Fabio BernardoniTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.
Maria SeidelTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.
Arne DooseTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.
Inger HellerhoffTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.ORCID http://orcid.org/0000-0002-6152-5834
Milena SchimackTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.
Jonas L SteinhäuserTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.ORCID http://orcid.org/0000-0001-5726-0928
Giulia LombardoDepartment of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.
Johanna L KeelerCentre for Research in Eating and Weight Disorders (CREW), Department of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.
David M PoitzInstitute for Clinical Chemistry and Laboratory Medicine, Faculty of Medicine, University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany.
Tjalf ZiemssenCenter of Clinical Neuroscience, Faculty of Medicine, University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany.
Kerstin WeidnerDepartment of Psychotherapy and Psychosomatic Medicine, Faculty of Medicine, University Hospital Carl Gustav Carus, TU Dresden, Dresden, Germany.ORCID http://orcid.org/0009-0007-9140-4068
Veit RoessnerGerman Center for Child and Adolescent Health (DZKJ), Partner Site Dresden/Leipzig, Dresden, Germany.
Joseph A KingTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany.ORCID http://orcid.org/0000-0002-2864-5578
Carmine M ParianteDepartment of Psychological Medicine, Institute of Psychiatry, Psychology & Neuroscience, King's College London, London, UK.ORCID http://orcid.org/0000-0002-9132-5091
Stefan EhrlichTranslational Developmental Neuroscience Section, Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, TU Dresden, Dresden, Germany. transden.lab@uniklinikum-dresden.de.ORCID http://orcid.org/0000-0003-2132-4445

Funding

Bundesamt für Berufsbildung und Technologie (Swiss Federal Office for Professional Education and Technology) SAXOCHILD 01GL2405ADeutsche Forschungsgemeinschaft (German Research Foundation) EH 367/5-1Deutsche Forschungsgemeinschaft (German Research Foundation) EH 367/7-1Deutsche Forschungsgemeinschaft (German Research Foundation) GRK2773/1-454245598Deutsche Forschungsgemeinschaft (German Research Foundation) SFB 940/2Else Kröner-Fresenius-Stiftung (Else Kroner-Fresenius Foundation) 2019_A118
6 · The paper itself

Abstract

Anorexia nervosa (AN) involves limbic dysfunction, yet its neurobiology remains unclear. Examining morphological alterations in subcortical limbic regions across AN's nutritional states and associations with neuroendocrine markers may improve understanding. We hypothesized that subcortical limbic volumes would be reduced in AN, normalize partially following short-term weight-restoration, and fully after long-term recovery. We examined whether leptin, ghrelin, neurofilament light (NFL), and brain-derived neurotrophic factor (BDNF) predict subcortical limbic dynamics. We studied 547 female individuals (aged 12-30 years): 168 with acute AN, 113 reassessed after ≈3 months of weight-restoration (>14% BMI increase), 80 long-term weight-recovered individuals, and 299 healthy controls. Ten subcortical limbic structures were segmented with FreeSurfer. Blood concentrations of leptin, ghrelin, NFL, and BDNF were measured. Group comparisons and marker associations were analyzed with mixed-effects models. Mediation was tested via regression-based mediation models. Most subcortical limbic volumes were reduced in AN (mean = -5.3%; Cohen's d-range = 0.24-0.76) but normalized after short-term weight-restoration (longitudinal change: mean = +5.8%; d-range = 0.30-0.56), except residual hypothalamic reductions. Rising leptin mediated weight gain-related volumetric increases in the left inferior tubular hypothalamus (proportion mediated = 52.8%) and left (96.7%) and right (156.8%) nucleus accumbens. Declining ghrelin mediated volumetric increase of the right nucleus accumbens (77.8%). Decreasing NFL following weight-restoration predicted increases in two hypothalamic subunits, the fornix, and right nucleus accumbens (d-range = 0.56-0.98). BDNF was unrelated to limbic dynamics. Subcortical limbic alterations in AN exceed other mental disorders, highlighting neuroplasticity. Neuroendocrine recovery (leptin and ghrelin) may reverse, and reduced axonal damage (NFL) may indicate neurostructural alterations in homeostatic and reward-related regions, with prognostic and therapeutic relevance in AN.

Indexed as

Anorexia NervosaGhrelinLeptinLimbic SystemNeurofilament ProteinsNutritional StatusAdolescentAdultBrain-Derived Neurotrophic FactorChildFemaleHumansMagnetic Resonance ImagingYoung AdultBDNF protein, humanBrain-Derived Neurotrophic FactorGhrelinLeptinneurofilament protein LNeurofilament Proteins

Identifiers

PMID42168586
PMCPMC13597489

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.