Anorexia nervosa (AN) is an eating disorder characterized by body weight loss, amenorrhea, and hyperactivity. It has the highest mortality rate of any psychiatric disorder and primarily affects young girls and women; however, increasingly, boys and men are also affected. Furthermore, brain volume loss has been associated with neuropsychological deficits in patients with AN. As with many psychiatric disorders, treatment options for AN are limited, and little is known about the underlying cellular and molecular biological mechanisms. Neurons and glial cells are becoming the focus of scientific interest.

To unravel the pathophysiology of AN, we use the murine starvation-induced hyperactivity (SIH) model, which mimics the somatic consequences of AN, such as body weight loss, hyperactivity, amenorrhea, and endocrine changes. This model involves providing an individually calculated restricted amount of food once a day and access to a running wheel. In this model, SIH mice receive 40% of their average daily food intake, calculated during an acclimatization phase, until a 25% body weight reduction is reached. This is followed by two weeks of daily food intake adjustments to mimic chronic starvation.

Our group focuses on investigating whether glial cell changes in the brain underlie the pathophysiology of AN. Additionally, we are interested in whether circadian changes and neurodegeneration contribute to the disorder. To address our scientific challenges, we use state-of-the-art methods such as an artificial intelligence infrared-sensory-based activity tracking system (Goblotrop), a set of behavioral analyses including the elevated plus maze and novel object recognition, and electron microscopy.