TL;DR
Dnmt3a dysregulation could be associated with altered OPC maturation and myelination in AMA offspring, possibly mediated by epigenetic mechanisms involving Olig2.
It is shown that trisomy 21 disrupts early developmental stages and establish oligodendrocyte enriched brain organoids as a human model to investigate the developmental origins of white matter and network dysfunction in DS.
These findings challenge an inflammation-centric interpretation of NPSLE hippocampal pathology, highlighting instead an additional contribution of impaired oligodendrocyte maturation.
Impaired myelination was observed in the cortex and hippocampus of the male FASD offspring, associated with hyperactivity‐like behaviors, whereas the female FASD mice exhibited delayed myelin formation and normal behaviors, indicating a gender‐specific manner of FASD pathology.
Prenatal maternal immune activation (MIA) during pregnancy is a prominent environmental contributor to neurodevelopmental disorders and psychiatric conditions in offspring, but the precise brain-region- and cell-type-specific mechanisms remain unclear. Using a lipopolysaccharide (LPS)-induced MIA mouse model, we show...
The results suggest that mid-gestation MIA may alter the development of deep-layer neurons through an epigenomic blockade of Tbr1 function, thereby perturbing normal cortical circuit formation.
Female offspring appear more vulnerable to pro-neurodegenerative changes, whereas male offspring activate compensatory neuroprotective pathways that might partially preserve hippocampal function despite sustained pro-inflammatory reactions, highlighting sex as a critical biological variable in the long-term consequence...
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