Double SHANK knockout highlights brain circuit’s social role
Mice missing the autism-linked SHANK2 and SHANK3 genes in their retrosplenial cortex have trouble distinguishing between novel and familiar mice.
Charting the structure and function of the brain’s many circuits may unravel autism’s mysteries.
Mice missing the autism-linked SHANK2 and SHANK3 genes in their retrosplenial cortex have trouble distinguishing between novel and familiar mice.
The transplanted cells integrate into living animals’ neural circuitry and influence behavior.
Common variants in five regions of the genome may determine whether someone has one condition versus the other.
Restoring the gene, TAOK2, in mice missing an autism-linked region of chromosome 16 normalizes neuronal movement during development.
After a brain transplant of reprogrammed human cells, the animals can for the first time recapitulate some neuronal changes seen in people with fragile X syndrome.
The results highlight the importance of subgrouping study participants based on their underlying genetics, the researchers say.
Non-neuronal brain cells called astrocytes secrete proteins that seem to hamper the growth of neurons in people with autism-related syndromes. These proteins could be new drug targets, Allen says.
The machine-learning approach could help identify how brain structure differs between autistic and non-autistic infants, the researchers say.
A well-studied brain response to sound appears earlier than usual in young children with autism.
Null and replicated results in this month’s newsletter tackle aging, a purported pathway for oxytocin’s effects on autistic people, and a possible autism biomarker.