Stanford researchers found that hyperactivity in the brain’s reticular thalamic nucleus causes autism‑like behaviors in mice. Dampening this overactivity—either with the experimental anti‑seizure drug Z944 or chemogenetic neuromodulation—reversed the behavioral deficits; ramping activity up in normal mice induced them. This ties autism‑like traits and epilepsy to a shared thalamic circuit.
— It reframes parts of autism as a reversible neural‑circuit dysfunction and flags anti‑epileptics and circuit‑level interventions as testable treatment paths rather than purely developmental labels.
Isegoria
2025.09.08
100% relevant
The team recorded RTN activity in Cntnap2 knockout mice and reported Z944 reversed behavioral deficits while DREADD suppression of RTN overactivity did the same.
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