Glucocorticoid signalling dysregulation and immune cell adaptation in Anorexia Nervosa.

Authors

Francesca Mottarlini, Lorenzo Da Dalt, Susanna Parolaro, Andrea Baragetti, Beatrice Rizzi, Sofia Taddini, Anna Chiara Cigognini, Francesca Vairano, Sara Bertelli, Armando D'Agostino, Fabrizia Bonacina, Giuseppe Danilo Norata, Fabio Fumagalli, Lucia Caffino

Published in

Molecular psychiatry. Jul 20, 2026. Epub Jul 20, 2026.

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.

PMID:
42477442
Bibliographic data and abstract were imported from PubMed on 21 Jul 2026.

Read full publication at:
Please sign in to see all details.

Stats

1-terrible, 9-excellent. How would you rate this publication? Sign in in to submit your rating.

Post a comment

You need to be signed in to post comments. You can sign in here.

Comments

There are no comments yet.