‘Splice-switching’ strategy boosts SYNGAP1 expression
The approach improves the function of SYNGAP1-deficient neurons in vitro, but whether it will work in people remains unclear.
The approach improves the function of SYNGAP1-deficient neurons in vitro, but whether it will work in people remains unclear.
A new gene therapy approach for epilepsy tamps down neural activity on demand.
The in-depth approach shows mutations in the autism-linked gene disrupt neuronal growth and communication, as well as mitochondrial gene expression.
The method yields complex organoids that more closely mimic embryonic brain development than do those cultured in other ways.
The model enables the study of autism-linked genes at the earliest stages of neural development.
Brain cell clusters serve as drug screens and reveal connectivity differences for autism-linked conditions, two new models show.
People with dup15q syndrome and those with idiopathic autism have similar patterns of altered gene expression in early brain development and later in life.
The developmental models have advantages over natural embryos and other synthetic models, such as organoids, but present technical and ethical challenges.
The transplanted cells integrate into living animals’ neural circuitry and influence behavior.
What these genes do and how they affect autism depends on when in development they’re studied, despite what classic ‘gene ontology’ analyses say.