Two roads diverge: Human brain organoids missing the gene TSC2 have overreactive astrocytes that are similar to those found in tubers from people with tuberous sclerosis complex, according to a new study. The findings substantiate the idea that glial pathology results from altered protein expression and activity—specifically, high mTORC1 signaling—rather than from seizures themselves. “These results implicate glial dysfunction as a driver of TSC pathogenesis and highlight reactive astrocytes as potential therapeutic targets for TSC-related neuropathology,” the investigators write.

Autism research spotted this week:

• “Postnatal maturation of putamen microstructure accompanies topographic white matter connectivity and altered circuits in autism” bioRxiv
• “A retinoic acid autoregulatory loop governing prefrontal-motor arealization” Nature
• “Developmental cerebellar pathology in mouse models of SCN2A premature termination codon variants” bioRxiv
• “Maternal-fetal immune conflict contributes to male-specific impairments in a mouse model of neurodevelopmental disorders” Science Advances
  See also: “Post-infection immune conflict alters fetal development in some male mice”
• “Parvalbumin interneurons and dentate gyrus homeostatic dysregulation shape epileptogenesis in Angelman syndrome model mice” bioRxiv