Dr Dierssen leads a Systems Neuroscience Lab at the Center for Genomic Regulation. She is interested in understanding how genetic perturbation in mental disorders modifies the way the brain integrates information. The main question in the field remains how the disturbances of dendritic tree architecture observed in most mental disorders constrain the network activity and influences cognition (Dierssen, 2012, Nat Rev. Neurosci). Dierssen lab uses a systems neuroscience approach that combines behavioral and molecular neurobiology analyses in genetic mouse models and cellular models. This systematic and wide-angled approach with different levels of description, has led them to build tools for gathering an integrated view of how the phenomic profiles correlate with cellular and molecular alterations in the neurons of these mouse models. This is a realistic stepping-stone towards unravelling the biological codes behind mental disorders.
Intellectual disabilities (ID) are chronic diseases that place a disproportionate burden on medical and social care, and educational systems, and rates of ID are on the increase. People with ID are vulnerable and many need lifelong assistance in most aspects of daily life. Cognitive deficits are a prominent feature and severely compromise their quality of life. The reduction in health inequalities and the improvement of health for people with intellectual disability has become a priority worldwide. In spite of the broad spectrum of genetic and environmental aetiologies, the disruption of neural plasticity can be viewed as a sign of cognitive impairment across ID. Our observations that brain plasticity is effective in the recovery from some of the cognitive deficits associated with ID open a window of opportunity for a novel therapeutic concept: therapies that improves and stabilizes physiological (experience-dependent) plasticity in genetic ID syndromes. Thus, targeting core molecular substrates of neuroplasticity with specific drugs, in combination with non-pharmacological interventions. We have identified an extremely powerful target for drug development, DYRK1A (dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A), a serine/threonine kinase that plays key roles in cell proliferation, survival and neural plasticity.