Analysis of cell death, oxidative stress and neuroinflammation in the hippocampus of mice with accelerated senescence after perinatal asphyxia

• Grant number: 24/10084-1
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Start date: September 01, 2024
• End date: August 31, 2025
• Field of knowledge: Biological Sciences - Morphology - Cytology and Cell Biology
• Principal Investigator: Silvia Honda Takada
• Grantee: Marina Diniz Barbezani
• Host Institution: Centro de Matemática, Computação e Cognição (CMCC). Universidade Federal do ABC (UFABC). Ministério da Educação (Brasil). Santo André , SP, Brazil

Abstract

Perinatal asphyxia, characterized by hypoxemia, hypercapnia, and acidosis, results from the partial or total interruption of oxygen supply, which may or may not be associated with ischemia, leading to hypoxic-ischemic brain injuries with a high incidence in premature newborns. Among survivors, 25% exhibit permanent neurological sequelae, such as learning difficulties, ADHD, and motor and cognitive deficits. Oxygen deprivation during the perinatal period triggers neurotoxic cascades, resulting in oxidative stress and neuroinflammation, which can persist throughout life and cause lasting damage to brain plasticity. This condition leads to continuous injury to the central nervous system, and recent studies suggest that perinatal asphyxia may contribute to or worsen neurodegenerative diseases, such as Alzheimer's disease (AD). In light of this, the project aims to standardize neonatal anoxia in SAMP8 and SAMR1 mice and assess cell death, oxidative stress, and neuroinflammation at different time points (48 and 72 hours post-asphyxia) as part of a larger project seeking to understand the effects of neonatal anoxia on the development of neurodegenerative diseases like Alzheimer's disease.