Autism’s genetic heterogeneity evident in brain connectivity patterns
The results highlight the importance of subgrouping study participants based on their underlying genetics, the researchers say.
The results highlight the importance of subgrouping study participants based on their underlying genetics, the researchers say.
The method, called Orgo-Seq, reveals that a deletion of genes on chromosome 16 increases the proportion of immature neurons and neural precursors in brain organoids derived from people with the mutation.
The cells’ altered proliferation rates hint at ways to diagnose and potentially treat autism earlier.
Of nine genetic models examined in a new study, all had some incidence of cardiac abnormalities. But the problems varied widely depending on the affected genes.
Scientists have at last filled in the missing gaps — an advance likely to inform every aspect of autism genetics research, Eichler says.
Some copy number variants may boost a person’s chances of having autism, but to a lesser extent than previously thought.
Over the past century, scientists have used a variety of animal models to advance their understanding of the developing brain and autism.
Inhibiting a protein that helps cells move or change shape prevents atypical neuronal migration in 3D clusters of brain cells carrying autism-linked genetic variants.
The finding that MDMA and an experimental serotonin agonist increase sociability across six different model mice suggests that disparate autism-linked mutations converge on the same underlying pathways.
An autism-linked mutation could make the brain grow unusually large by prompting cells to express a chemical signal better known for its connection to cancer.