| Grant number: | 19/25957-2 |
| Support Opportunities: | Regular Research Grants |
| Start date: | February 01, 2021 |
| End date: | January 31, 2024 |
| Field of knowledge: | Biological Sciences - Biochemistry - Chemistry of Macromolecules |
| Agreement: | Max Planck Society for the Advancement of Science |
| Principal Investigator: | Daniel Martins-de-Souza |
| Grantee: | Daniel Martins-de-Souza |
| Principal researcher abroad: | Reinhard Jahn |
| Institution abroad: | Max Planck Society, Gottingen , Germany |
| Host Institution: | Instituto de Biologia (IB). Universidade Estadual de Campinas (UNICAMP). Campinas , SP, Brazil |
| City of the host institution: | Campinas |
Abstract
Schizophrenia is a severe mental disorder that affects 0.7% of the worldwide population. The interactions between genetic and environment factors seem to be responsible for alterations in neurodevelopment, resulting in the manifestation of schizophrenia in late adolescence to early adulthood. The pathophysiology of schizophrenia is highly complex and involves several neurotransmission systems. To change these conditions, it is necessary to understand the pathophysiology of schizophrenia at the molecular level. Besides the long-established neurodevelopmental hypothesis, studies focusing on neuroimaging, postmortem brain proteomics, and pharmacological, genetic, and animal model studies have shown deficits in synaptic transmission. As all these factors may be connected in the etiology of this disorder, we intend to integrate the state-of-the-art approaches of synaptic vesicle function, neuroproteomics, and pluripotent stem cells to further investigate the biological mechanisms involved in synaptic dysfunction during the course of neurodevelopment in schizophrenia, along with the potential treatments for this disorder. (AU)
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