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Maternal-fetal type I interferon signaling drives TREM2 dysregulation and synaptic dysfunction in neurodevelopmental disorders.
Neuron · · Journal Article · Open access
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Abstract ↗AI summary
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Maternal type I interferon signaling causes TREM2 dysregulation and synaptic dysfunction in offspring hippocampus in a neurodevelopmental disorder model.
- Why it matters: Understanding how maternal infections influence neurodevelopment is crucial because they increase the risk of disorders like schizophrenia, but the underlying immune mechanisms remain unclear.
- What they did: Using a maternal immune activation model with poly(I:C), the study examined hippocampal changes, revealing increased maternal IFN-I, reduced TREM2 expression in microglia, and disrupted synaptic homeostasis in juvenile offspring.
- The result: Blocking maternal IFN-I signaling restored TREM2 function and synaptic integrity, indicating that targeting IFN-I pathways during pregnancy could help prevent neurodevelopmental dysfunctions.
The findingWhy it mattersWhat they didThe result
- Open access
- 2 cites