Increasing or reducing the levels of the UBE3A gene, which is associated with autism and autism-related syndromes, results in altered patterns of synaptic pruning — a process that snips away brain cell connections.

This month’s Going on Trial newsletter dives into an electroencephalography biomarker that could track the efficacy of treatments for dup15q and Angelman syndromes, among other drug development news.

Brain scans of hundreds of infants suggest that up to 80 percent of those with autism have unusual amounts of cerebrospinal fluid. Researchers are studying how this might contribute to the condition.

The mutation increases the activity of an autism-linked protein and leads to social difficulties and other behavioral differences in mice.

This month’s issue of the Null and Noteworthy newsletter breaks down some negative results involving prenatal exposures, an experimental treatment for Angelman syndrome, and the role that age at autism diagnosis plays in subsequent outcomes, and more.

Here is a roundup of news and research for the week of 26 June.

If a therapy for autism’s core traits makes it to market, it will likely take one of three forms, the researchers say.

The result raises hopes for an ongoing clinical trial in people — and offers fresh insight into the biology of imprinting and the UBE3A antisense transcript.

UBE3A, a key gene associated with both autism-linked conditions, can explain most — but not all — of the syndromes’ atypical neuronal properties.

The treatment eases the animals’ sleep troubles, suggesting it has clinically meaningful effects beyond what was thought to be a critical window in early life.