My research activity is focused on the study of iron metabolism in the Central Nervous System (CNS) in the context of aging and neurodegenerative diseases, especially Alzheimer’s disease (AD). During my PhD at the University of Torino, I worked on the molecular characterization of iron metabolism in mice brain during aging to better understand if systemic iron regulation is also active in the brain. Indeed, brain iron accumulation due to iron dyshomeostasis is a typical pathological feature of aging and several neurodegenerative disorders. In this study, I identified a remarkable reduction of Zonula occludens1 (ZO-1), a tight junction protein of the Blood-Brain Barrier (BBB), indicating an increased permeability to iron in old mice. Moreover, I observed the alteration of iron homeostasis and its deposition in the brain driving neuroinflammation and oxidative stress. Importantly, I found that the iron regulator pathway Hepcidin/Ferroportin (Fpn1) is activated in the brain as consequence to the increase of iron content, and it results in the inhibition of the iron exporter Fpn1. Enthusiastic and highly motivated by these results, that have been recently published in Scientific Reports (Mezzanotte M, et al. Sci Rep. 2022 Jul 9;12(1):11724. doi: 10.1038/s41598-022-15812-4), I'm continuing as an early postdoc fellow at the Institute of Neuroscience Fondazione Cavalieri Ottolenghi (University of Turin) focusing on iron metabolism in the regions most affected by neurodegeneration, the Cerebral Cortex and Hippocampus, of Alzheimer's animal models. The main goal is to study: the effect of intracerebral iron changes ex vivo by measuring the main proteins involved in iron metabolism and mitochondrial activity; the effect of in vivo drug administration on brain iron levels, cognition and locomotion and to carry out advanced imaging experiments to trace the mitochondrial activity in the brain of mice.