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Peer-reviewedCC BY 4.0Molecular Psychiatry

Glucocorticoid signalling dysregulation and immune cell adaptation in Anorexia Nervosa

  • Francesca Mottarlini1
  • Lorenzo Da Dalt1
  • Susanna Parolaro1
  • Andrea Baragetti1
  • Beatrice Rizzi1,2
  • Sofia Taddini1
  • Anna Chiara Cigognini3
  • Francesca Vairano3
  • Sara Bertelli3
  • Armando D’Agostino3,4
  • Fabrizia Bonacina1
  • Giuseppe Danilo Norata1
2 more authors
  • Fabio Fumagalli1
  • Lucia Caffino1
4 affiliations
  1. 1Department of Pharmacological and Biomolecular Sciences “Rodolfo Paoletti”, Università degli Studi di Milano, Via Balzaretti 9, 20133 Milan, Italy
  2. 2Center for Neuroscience, University of Camerino, Camerino, Italy
  3. 3Department of Mental Health and Addiction, Asst Santi Paolo e Carlo, Milan, Italy
  4. 4Department of Health Sciences, Università degli Studi di Milano, Milan, Italy
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Abstract

Anorexia Nervosa (AN) is a neuropsychiatric disorder marked by compulsive weight-loss and hyperactivity, with poorly understood underlying mechanisms and limited treatment outcomes. Here we show that women with AN, at the first medical evaluation, exhibit hyperactivity and hypercortisolemia, together with a reduced immune cell count yet paradoxically showing increased levels of cell activation. One year later, only subjects considered in remission showed greater increases in cortisol and cytokine levels, along with enhanced monocyte differentiation and recruitment. Using the activity-based anorexia (ABA) rat model, we reproduced AN core features, including hypercorticosteronemia, and observed innate-skewed immune profiles, as well as persistent microglial and glucocorticoid receptor (GR) dysfunction in the ventral hippocampus. Pharmacological blockade of GR with RU486 attenuated hyperactivity and reshaped microglial phenotype in the ventral hippocampus. Our results suggest that cortisol elevation and immune cell adaptation may perpetuate disease vulnerability beyond weight normalization, challenging the notion of weight regain as an indicator of remission.

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Cite

BibTeXRIS
BibTeX
@article{mottarlini2026glucocorticoid,
  title = {{Glucocorticoid signalling dysregulation and immune cell adaptation in Anorexia Nervosa}},
  author = {Francesca Mottarlini and Lorenzo Da Dalt and Susanna Parolaro and Andrea Baragetti and Beatrice Rizzi and Sofia Taddini and Anna Chiara Cigognini and Francesca Vairano and Sara Bertelli and Armando D’Agostino and Fabrizia Bonacina and Giuseppe Danilo Norata and Fabio Fumagalli and Lucia Caffino},
  journal = {Molecular Psychiatry},
  year = {2026},
  month = jul,
  doi = {10.1038/s41380-026-03756-4},
  url = {https://doi.org/10.1038/s41380-026-03756-4},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Glucocorticoid signalling dysregulation and immune cell adaptation in Anorexia Nervosa
AU  - Francesca Mottarlini
AU  - Lorenzo Da Dalt
AU  - Susanna Parolaro
AU  - Andrea Baragetti
AU  - Beatrice Rizzi
AU  - Sofia Taddini
AU  - Anna Chiara Cigognini
AU  - Francesca Vairano
AU  - Sara Bertelli
AU  - Armando D’Agostino
AU  - Fabrizia Bonacina
AU  - Giuseppe Danilo Norata
AU  - Fabio Fumagalli
AU  - Lucia Caffino
PY  - 2026
DA  - 2026/07/20
JO  - Molecular Psychiatry
DO  - 10.1038/s41380-026-03756-4
UR  - https://doi.org/10.1038/s41380-026-03756-4
AB  - Anorexia Nervosa (AN) is a neuropsychiatric disorder marked by compulsive weight-loss and hyperactivity, with poorly understood underlying mechanisms and limited treatment outcomes. Here we show that women with AN, at the first medical evaluation, exhibit hyperactivity and hypercortisolemia, together with a reduced immune cell count yet paradoxically showing increased levels of cell activation. One year later, only subjects considered in remission showed greater increases in cortisol and cytokine levels, along with enhanced monocyte differentiation and recruitment. Using the activity-based anorexia (ABA) rat model, we reproduced AN core features, including hypercorticosteronemia, and observed innate-skewed immune profiles, as well as persistent microglial and glucocorticoid receptor (GR) dysfunction in the ventral hippocampus. Pharmacological blockade of GR with RU486 attenuated hyperactivity and reshaped microglial phenotype in the ventral hippocampus. Our results suggest that cortisol elevation and immune cell adaptation may perpetuate disease vulnerability beyond weight normalization, challenging the notion of weight regain as an indicator of remission.
SN  - 1359-4184
SN  - 1476-5578
ER  -