Evidence has shown that inflammation can contribute to the development of psychiatric and neurodegenerative disorders, such as unipolar and bipolar depression, schizophrenia and Alzheimer's disease. Patients suffering from these disorders show higher levels of both body and brain inflammation. In particular, inflammation in the brain can impair the ability to generate new neurons, a process called neurogenesis, or can contribute to the death of existing neuronal cells. Reduced neurogenesis and neuronal cell death are both fundamental processes ultimately leading to neurodegeneration and long-term cognitive impairments in patients. Indeed, the association between psychiatric symptoms that often develop during adolescence or middle age, and the neurodegenerative diseases that occur later in life are supported by various lines of evidence. However, the exact way through which inflammation detrimentally affects the brain and its neurogenesis processes in patients with neuropsychiatric and neurodegenerative disorders it is still to be fully understood. 

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Our first aim is to assess changes in neurogenesis upon exposure of human brain neurons to specific immune-related proteins, also called cytokines, which were previously identified among patients suffering from neuropsychiatric and neurodegenerative disorders. Subsequently, we will investigate which genes are involved in the changes observed in neurogenesis, and caused by the cytokines. Finally, we will test the ability of pharmacological drugs, including those commonly administered to patients with neuropsychiatric and neurodegenerative disorders, to either reduce or prevent these detrimental changes. Our ultimate goal is to identify novel mechanisms through which inflammation affects the brain of patients with neuropsychiatric and neurodegenerative disorders, and ultimately to contribute to the development of novel and more personalised treatment strategies able to target those mechanisms and to prevent progression of these conditions. We believe that investigating inflammation as a transdiagnostic mechanism will deliver novel advances that go beyond disorder-specific studies.

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