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Research mission

 

More than any other species, humans are beneficiaries and victims of emotion. The pivotal role that emotion plays in our life is evident in that what we notice and remember is not the mundane but events that evoke feelings of joy, sorrow, pleasure, or fear. A lack of emotional equilibrium has debilitating impact on human cognition and behavior and is central to depression and anxiety, which are the most common psychiatric disorders. Depression is the leading source of medical disability for people under age 45 in the developed world. For those affected, depression means hopelessness, helplessness, anhedonia, a deep sense of despair, and a wide range of physical symptoms. Comorbidity between depression and anxiety is the rule and not the exception, with approximately 90% of anxiety patients experiencing depression at some point in their lifetime. Unfortunately, up to 30% of patients with depression and anxiety do not respond to standard medication and cognitive behavioral therapy (CBT). Unravelling the pathophysiological substrates of depression and anxiety, and developing new treatments targeting these substrates, thus is of tremendous importance. Converging evidence suggests that there are specific circuits in our brain that mediate stress responsiveness and regulate emotional and cognitive functions. Depression and anxiety represent brain-based disorders that lead to dysregulation of these neural circuits. NEMO lies its focus on new pharmacological and neuromodulatory therapies addressing these networks in order to establish more rapid and robust methodologies for treating depression and anxiety. By pursuing clinical studies in patients and preclinical studies in healthy volunteers, NEMO uses an integrative translational research strategy («from bedside to bench and back again»). Methodologically, NEMO combines insights from behavioral neuroscience, functional neuroimaging (including pharmacological fMRI and radioligand PET), and brain stimulation techniques (including MRI-navigated rTMS and tDCS).