The main objective of the project consists in characterization of persistent negative symptoms in a transdiagnostic sample of subjects with SMI and the investigation of distinct pathophysiological mechanisms underlying the different domains of negative symptoms.
The specific objectives of the project are:
SO1. Development of a psychiatric tool for investigation of neurocognitive and social cognitive.
SO2. Development of the expressive deficit domains, tests on the hypothesis of association with signs of altered neurodevelopment.
SO3. Validation of hypotheses and identify possible biomarkers of the negative symptom domains, collection of resting state and task-related electrophysiological and brain imaging data in patients with SMI.
SO4. Design the animal modelling to validate possible genetic and molecular pathophysiological mechanisms underlying the neurobiological abnormalities associated with the different domains of negative symptoms.
SO5. Development of HR competence (encouraging the formation of researchers in a high-quality scientific environment): cumulated 2 FTE for PhD students and cumulated 2 FTE for post-Doc researchers.
Project executive summary
Negative symptoms occur in several psychiatric disorders and are associated to poor functional outcome. In severe mental illnesses (SMI), such as schizophrenia, bipolar disorder and unipolar depressive disorder, these symptoms represent an unmet need of the treatment. These symptoms cluster in the expressive domain (including anhedonia, avolition and asociality) and the expressive one (blunted affect and alogia). Advance in the understanding of the pathophysiological mechanisms underlying these domains is needed to develop innovative treatments.
The main objectives of the present study include the characterization of persistent negative symptoms in a transdiagnostic sample of subjects with SMI and the investigation of the pathophysiological mechanisms underlying the different domains of negative symptoms. We will investigate the association of the experiential domains with alteration of reward processing and motivational deficits, as well as the interactions of these neurobiological dysfunctions with neurocognitive and social cognitive deficits. For the expressive deficit domains, we will test the hypothesis of association with signs of altered neurodevelopment, i.e., neurological soft signs and generalized reduction of cognitive abilities. Resting state and task-related electrophysiological and brain imaging data will be collected in patients with SMI to test the above hypotheses and identify possible biomarkers of the negative symptom domains. Translational animal models will validate possible genetic and molecular pathophysiological mechanisms underlying the neurobiological abnormalities associated with the different domains of negative symptoms.