A new gene-editing system allows researchers to rewrite lengthy stretches of DNA in zebrafish and identify the mutant fish with ease.
A drug that mimics estrogen eases hyperactivity in zebrafish lacking the autism-linked gene CNTNAP2. The results highlight the potential of the tiny fish for screening autism treatments.
A new technique gives researchers a window into the constellation of neurons that fire as zebrafish larvae swim in a dish.
Mutations in a section of chromosome 16 that is linked to autism have an unexpected effect: They alter the miniscule hairs, or cilia, that adorn the surface of all cells. The findings suggest that problems with these cilia may contribute to autism.
There is some evidence that neural habituation — the process by which neurons get used to sensory stimuli — goes awry in autism. Mutant fish may help us understand the sensory sensitivities that often accompany the disorder, says Alan Packer.
Missing a swath of chromosome 16 with strong ties to autism disrupts proteins crucial for early brain development. The findings open the door to targeted interventions.
Looking in families with a history of severe autism among women, researchers have unearthed 18 new candidate genes for the disorder. One of these genes, delta-catenin, plays a critical role in brain development, researchers reported yesterday in Nature.
Scientists peel back the layers of genetic complexity in autism, starting with the master regulator CHD8.
After eight years of prominence as an autism risk gene, a new analysis significantly brings down CNTNAP2’s importance in the disorder: According to the study, rare mutations in a single copy of the gene are unlikely to cause autism.