Survivors of pediatric central nervous system (CNS) tumors treated with radiation therapy demonstrate neurocognitive impairment-linked with underscored educational deficits and occupational attainment at adulthood. Exposure of the brain at young age to radiation is known to damage several cell populations. Several studies have already revealed that ionizing radiation ‘IR’ interferes with hippocampal neurogenesis by inducing cell death of neuronal precursor stem cells (NPCs), reducing the survival rate of proliferating neurons and inducing neuroinflammation. Contributing thus to impaired cognition at adult age. In this project, we will characterize the cellular events and molecular pathways leading to cognitive defects in animal models following exposure to radiation at young age, to identify predictive molecular biomarkers of cognitive impairment. Besides, the major aim of this project is to identify potential countermeasures capable to interfere with the above pathways and biomarkers to preserve cognition at adulthood by preventing neural stem cell damage following radiation exposure, as well as by improving neuronal maturation, migration and renewal of dead cells. As such, this project will help to elucidate the potential damaging effect of radiation on the brain of young animals at high and at low doses. Additionally, this project aims at identifying countermeasures in animal models to mitigate brain damage, which can later be used for humans to improve the quality of life of children at risk for developing cognitive impairment.