A genetic mutation linked to intellectual disability and autism causes the premature formation of functional connections between brain cells during a crucial window of development early in life.

Mutations that inactivate one copy of the gene SYNGAP1 often cause intellectual disability in humans. Gavin Rumbaugh of the Scripps Research Institute in Jupiter, Florida, and his team found that mice with a similar mutation produce neurons that mature too quickly after birth and become overactive in a brain region important for cognitive function. Mice with one copy of SYNGAP1 have memory problems and are prone to seizures — a symptom in humans with the mutations.

Correcting the mutation in mice after this developmental period had little effect on the symptoms, and introducing the mutation into adult mice did not affect neuronal function — suggesting that the activity of the SYNGAP1 protein during this developmental window has long-lasting effects.

Cell 151, 709–723 (2012)