Roger Adan
About
Since 2002 I am a full professor in molecular pharmacology at the department of neuroscience and pharmacology of the University Medical Center Utrecht and my research is embedded in the Rudolf Magnus Institute of Neuroscience (http://www.rudolfmagnus.nl/). We aim at unraveling the genetic and neural pathways underlying eating disorders and obesity. Feeding behavior is a complex behavior that serves to control energy balance of an organism. Homeostatic control over energy balance is challenged by higher brain centers that drive feeding of palatable foods or inhibit feeding in order to loose weight. These disruptions may contribute to development of eating disorders and obesity. Several animal models are used in which anorectic behavior (including hyperactivity) is mimicked or in which animals become obese following exposure to palatable choice diets. Using viral vector technology, genes are either overexpressed or knocked down (RNAi) in these animals, in order to unravel the role of genes in feeding behavior and energy balance. Results from animal experiments are translated into clinical relevance by using a human genetics approach. DNA from eating disorders patients and epidemiological cohorts is available with extensive phenotypic information. This allows to determine genotype-phenotype relationships in humans. Since 2010 I also hold a research position at Rintveld Eating disorders which ensures the translational character of the eating disorder research line.
Publications
- Overview of genetic research in anorexia nervosa: The past, the present and the future.
- Evidence for three genetic loci involved in both anorexia nervosa risk and variation of body mass index.
- Insensitivity to Losses: A Core Feature in Patients With Anorexia Nervosa?
- Disordered eating in three different age groups in Cyprus: a comparative cross-sectional study.
- The determinants of food choice.
- Eating disorders: the big issue.
- Associations between neural correlates of visusal stimulus processing and set-shifting in ill and recovered women with anorexia nervosa.
- Altered food-cue processing in chronically ill and recovered women with anorexia nervosa.
- Drive for activity in patients with anorexia nervosa.
- Longitudinal changes in the physical activity of adolescents with anorexia nervosa and their influence on body composition and leptin serum levels after recovery.
- The Val66Met polymorphism of the BDNF gene in anorexia nervosa: new data and a meta-analysis.
- Neuropsychological weaknesses in anorexia nervosa: set-shifting, central coherence, and decision making in currently ill and recovered women.
- Hyperactivity in anorexia nervosa: Warming up not just burning-off calories.
- Anorexia nervosa and the Val158Met polymorphism of the COMT gene: meta-analysis and new data.
- Mandometer treatment not superior to treatment as usual for anorexia nervosa.
- A meta-analysis of circulating BDNF concentrations in anorexia nervosa.
- Are recently identified genetic variants regulating BMI in the general population associated with anorexia nervosa?
- Leptin’s effect on hyperactivity: potential downstream effector mechanisms.
- A polymorphism in the 3′ untranslated region of the CCK gene is associated with anorexia nervosa in Dutch patients.
- Mutation analysis of the agouti related protein promoter region and the melanocortin-3 receptor in anorexia nervosa patients.
- Olanzapine reduces physical activity in rats exposed to activity-based anorexia: possible implications for treatment of anorexia nervosa?
- Polymorphisms in the brain-derived neurotrophic factor gene are not associated with either anorexia nervosa or schizophrenia in Dutch patients.
- Refinement of behavioural traits in animals for the genetic dissection of eating disorders.
Click here to view my articles on pubmed.