Topic: oligodendrocyte differentiation

The neural basis of abnormal social behavior in autism spectrum disorder (ASD) remains incompletely understood and previous studies has highlighted that altered myelination could be involved in the pathophysiology of ASD. We have characterized the myelination process during development in the cntnap2-/- mouse model of ASD. We observed that oligodendrocyte differentiation and myelination are transiently impaired during cortical development in cntnap2-/- mice. Thus, we observed a reduction in myelinated fibers, the number of nodes of Ranvier and the proportion of mature oligodendrocytes in somat

Early life adversity (ELA), defined as an adverse experience during critical periods in brain development, is a risk factor for neurodevelopmental and psychiatric disorders. The major effector molecules of stress are glucocorticoids (GCs), which by binding to glucocorticoid receptors (GRs) regulate several biological processes in the brain and the body. So far, little is known about the effects of ELA on a subtype of glial cells, named oligodendrocyte precursor cells (OPCs) or NG2-glia. To investigate how GCs can affect the molecular signature of the NG2-glia and impact the behavioral phenotyp

White matter injury (WMI) is frequently observed in preterm infants, despite advances in neonatal care. Hypoxia is a key contributing factor which, through heightened vulnerability of preterm newborns, leads to oligodendrocyte dysmaturation, ultimately impairing essential myelination processes. To date, no known effective treatment exists. Considering our recent finding, that inhibiting GPR17 enhances oligodendrocyte progenitor cell (OPC) differentiation and myelination following optic nerve crush, we aimed to investigate the impacts of genetic and pharmacological manipulation in a WMI model.C