Inflammatory mechanisms in long-term cognitive deficits induced by perinatal asphyxia

Hypoxic-ischaemic encephalopathy (HIE), a condition caused by oxygen deprivation around birth, accounts for the death of around one million newborns worldwide every year, and the number of neonates who suffer permanent neurological damage is much higher. Even with a mild course, HIE can lead to long-term neurodevelopmental, behavioural, cognitive and psychiatric disorders. The aim of our research is to identify potential new therapeutic targets and biomarkers that may predict increased risk for subsequent psychiatric disorders by translational preclinical investigation of the brain disease mechanisms underlying the long-term effects of HIE.

In a novel translational rodent model of perinatal oxygen deprivation, we have recently explored the inflammatory mechanisms underlying neurological damage and their long-term consequences for cognitive, emotional, social and neuromotor functioning. Currently, we are investigating functional connectivity abnormalities related to behaviour and searching for predictive markers of early physiological and neurological status and emotional reactivity for the onset of later behavioural disorders, using targeted neurobehavioural manipulation techniques combined with complex behavioural studies, RNAseq, confocal and super-resolution microscopy.

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