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1. Attention deficit hyperactivity disorder (ADHD) and associated neurodevelopmental disorder: mechanism and therapy
We are interested in the (epi)genet and environmental risk factors of ADHD and related neurodevelopmental disorder. Genotyping and epigenetic analysis of relevant genes and polygenic risk factors (PRS) are investigated to elucidate their association with attention or/and hyperactivity phenotypes.
The aim is to uncover the etiopathology of the disorder, identify new therapeutic targets and predict the persistence of the disorder.In addition, we have initiated a project in which we are investigating the relationship between ADHD and dementia over the entire lifespan of an individual, based on the "last in, first out" hypothesis, which suggests that comparable signalling pathways are active in both disorders.
The mechanism of action of drugs used for ADHD treatment, e.g. methylphenidate (Ritalin) and Atomoxetine are studied to better understand the long term effects and the molecular and cellular causes for non response.
Moreover, alternatives, such a unsaturated fatty acids (omega-3) are investigated as alternative or add-on to the standard therapy. To investigate the cellular and molecular alterations causing ADHD and neurodevelopmental delays, we use induced pluripotent stem cells (iPSC) generated from patients and controls, differentiated into brain cells.
2. Obsessive Compulsive disorders (OCD) and related disorders (OCRD)
Similarly to ADHD we aim to elucidate the genetic x environmental role of the two in the disorder and their therapy response.
Both genetic and epigenetic bromarkers are assessed combining clinical phenotypes, severity (CY-BOCS) and therapy response in order to elucidate subgroups. Modeling OCD in a dish, using iPSC- derive neurons, opens the opportunity to elucidate the cellular and molecular mechanism, and the etipoathogenesis of the disorder, as well as the molecular pathways leading to therapy resistance.