This symposium is dedicated to new insights from neurobiological research into underlying mechanisms and principles of anorexia nervosa (AN) and what we can learn from it for clinical practice. First Mrs Janet Treasure, UK, will open by giving an overview over previous research regarding neuroprogressive changes in patients with AN getting worse as the illness protracts over time into chronicity and with longer illness duration being an important predictor for a more direworse outcome. Social cognition appears especially affected disturbing interpersonal functioning and impacting relations with close others. She suggests a new staging model of AN with implications for differential treatment of acute and chronic patients targeting a range of maintaining factors that emerge as a consequence of neuroprogressive changes from protracted starvation. Ms Ida Wessing, Germany, will try to elucidate one of those maintaining factors by focussingfocusing on the motivational responses to food in patients with AN using highly time-sensitive magnetoencephalography. She could show enhanced early bottom-up driven but reduced later more top-down controlled brain activity. This suggests enhanced first motivational orienting towards food stimuli which then are cognitively overregulated. Mr. Sebastien Guillaume, France, will present brand new epigenetic results reflecting which genes are activated and which are silenced by methylation in patients AN cross-sectionally and longitudinally. He found differentially activated genes in AN patients vs controls and during weight gain, differing between those patients with good vs bad prognosis. Involved genes pertain to brain development and plastisticity, potentially explaining underlying psychopathology. Finally, Mr Jochen Seitz, Germany, will present his talk on the cause and effect of brain volume loss in AN using human and animal data. He could show that brain volume loss is associated with neuropsychological deficits and worse clinical prognosis. New animal results show an almost 50% reduction in astrocyte number and volume in gray and white brain matter. As astrocytes directly influecence neuronal function, this could help explain neuropsychological deficits and give rise to astrocytes as new research target, e.g. by using estrogen replacement therapy.