The involvement of brain norepinephrine nuclei in eating disorders

While many individuals with anorexia nervosa (AN) undergo remission of the disorder, a significant proportion will experience relapse and/or persistent symptoms. The persistence of AN is thought to be driven by changes in neural circuits that underline treatment-resistant symptoms (maladaptive plasticity). Recent evidence about the biology of AN suggests it extends beyond psychiatric symptoms to involve also systemic metabolic dysfunction, which is based on alterations of the mechanistic Target Of Rapamycin Complex 1 (mTORC1). In this review, we propose that AN's maladaptive plasticity and mTORC1 alterations involve norepinephrine (NE) nuclei, which spread neurobiological alterations concomitantly to the forebrain as well as to peripheral organs through the autonomic nervous system. In this review, we will present current evidence supporting this new perspective about the role of NE neurons in producing the psycho-metabolic dysfunction occurring in AN and discuss how it may inform more effective treatments for AN in the future.