Key role of interferon 1 in maternal immune activation, and more

Immune power: Maternal-fetal type 1 interferon may be a key factor in the association between maternal infection during pregnancy and having an autistic child, according to a new mouse study. Maternal immune activation, modeled in mice, increased interferon 1, which, in offspring, altered excitatory synapse function and reduced a microglial regulator of synapse formation. Further, blocking interferon 1 signaling restored these effects on synapses. The Transmitter has reported on the idea that some women have a genetic predisposition that contributes to the infection-autism association. The new findings suggest that monitoring the cytokine during pregnancy may help identify—and potentially treat—those that have elevated chances of having a baby with a neurodevelopmental condition. 

Autism research spotted this week: 

“Appraising familial prediction of proband outcomes in neurogenetic disorders” medRxiv
See also: “Extra Y chromosomes are linked to autism
“Convergent and divergent brain-cognition development in early adolescence” Nature Communications
“CSNK2B gene replacement rescues autism-related phenotypes and establishes translational EEG biomarkers” Cell Reports Medicine
“Recurrent copy number variants and psychiatric outcomes in the context of polygenic scores” JAMA Psychiatry
“Defective ventral neurogenesis due to midfetal CHD8 mutation drives autistic-like behavior in mice” Nature Communications
“Changes in the profile of adults diagnosed as autistic since 2010: Population based studies in the United Kingdom and Sweden” medRxiv
“Limited discrepancy between cognitive ability and daily living skills in autism: A longitudinal study from ages 2-25” Autism Research