Effect of chronic caffeine intake on changes behavioral, cognitive and molecular resulting from the LPS-induced neuroinflammation.

• Grant number: 22/15966-7
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: December 01, 2023
• End date: November 30, 2024
• Field of knowledge: Biological Sciences - Biochemistry - Molecular Biology
• Principal Investigator: Rodrigo Augusto da Silva
• Grantee: Kassia de Carvalho
• Host Institution: Vice-Reitoria de Pesquisa e Pós-Graduação. Universidade Paulista (UNIP). São Paulo , SP, Brazil

Abstract

Caffeine is the most consumed psychoactive substance in the world, present in several plants and products. Numerous studies have demonstrated the multidirectional influence on various organs of the human body, with its long-term intake correlated by longitudinal studies as a protective factor against cognitive decline by attenuating neurotoxicity associated with oxidative stress and inflammatory processes related to the aging process. However, the molecular and epigenetic pathways modulated by its regular consumption still remain unclear. In this sense, this study aims to determine the neuroprotective potential of chronic caffeine treatment in a murine model of neuroinflammation induced by lipopolysaccharide (LPS). For this, Black C57 (C57/BL6) mice will be used, which will have free access to caffeine (0.5 mg/L) prepared in sterilized water for 12 weeks. During this period, the consumption of the caffeine solution will be measured daily and the other parameters: body weight and behavioral development parameters will be measured once a week and behavioral tests related to anxiety and learning/memory will be observed every 2 weeks. After chronic caffeine ingestion (12 weeks), neuroinflammation will be induced through intraperitoneal (i.p.) administration of a single injection of LPS (0.5 mg/kg) and brain structures will be collected after 24 h. Molecular and epigenetic analyzes will be carried out to determine the transcriptional profile and methylation status of the promoter region of genes encoding inflammatory cytokines and genes encoding Adenosine receptors type A1 and 2A.