Grant number: | 24/09209-4 |
Support Opportunities: | Scholarships in Brazil - Doctorate |
Start date: | March 01, 2025 |
End date: | May 31, 2028 |
Field of knowledge: | Biological Sciences - Physiology - Physiology of Organs and Systems |
Principal Investigator: | Fulvio Rieli Mendes |
Grantee: | Alessandra Aparecida Marques |
Host Institution: | Centro de Ciências Naturais e Humanas (CCNH). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil |
Associated research grant: | 22/12675-1 - Potential therapeutic action and mechanisms of action of adaptogenic plants in neurodegenerative diseases, AP.BTA.R |
Abstract Neuroinflammation and oxidative stress are elements present in the vast majority of pathological conditions. Therefore, substances capable of modulating anti-inflammatory and oxidative pathways have been considered as a promising strategy to attenuate these processes and, consequently, reduce symptoms and delay the progression of neurodegenerative diseases and other psychopathologies. In this context, recent studies have pointed to the unique characteristic of ketamine, which is to act as an anti-pro-inflammatory drug, capable of preventing the generalization of neuroinflammation without preventing local inflammatory processes important for homeostasis. However, the mechanism of action by which this effect occurs is unclear. Therefore, this study aims to investigate the possible therapeutic effects of ketamine in a model of neuroinflammation induced by lipopolysaccharide (LPS), with emphasis on the modulation of the inflammatory and oxidative response by nuclear factor erythroid 2-related factor 2 (Nrf2). For this purpose, in vitro and in vivo experiments will be conducted, aiming to integrate cellular and behavioral data to investigate the mechanisms of action of ketamine in the context of neuroinflammation and oxidative stress. The results of this study may contribute to the understanding of the therapeutic potential of ketamine and to the elucidation of possible pathways involved in cytoprotection, thus providing support for the development of new therapeutic approaches. | |
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