Topic: neonatal seizures

Birth asphyxia (BA) is one of the most serious birth complications affecting infants and can result in severe disabilities including mental retardation, cerebral palsy, and epilepsy. Animal models of BA and subsequent hypoxic-ischemic encephalopathy (HIE) are important to characterize functional and behavioral correlates of injury, explore underlying mechanisms, and assess the potential of novel therapeutic strategies. Using a non-invasive, physiologically validated rat model of BA and acute neonatal seizures that mimics many features of BA and HIE in human infants we studied (i) the temporal

Developmental and epileptic encephalopathies (DEE) are a spectrum of severe neurological disorders with poorly understood aetiologies, often involving metabolic dysfunctions. Biallelic recessive pathogenic variants in the Solute carrier family 13 member 5 gene (SLC13A5) gene cause a severe form of DEE, characterized by intractable neonatal seizures, developmental delay, and tooth hypoplasia. SLC13A5 encodes the sodium-dependent citrate transporter (NaCT) on the plasma membrane, expressed in brain and liver. Recent investigations highlighted the relevance of NaCT in citrate uptake, influencing