Synaptic Pruning Improves Autism in Mice

Fixing impaired pruning and autophagy signaling in neurons eases the symptoms of autism in a mouse model of the disorder.

Written byKerry Grens
| 2 min read

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WIKIMEDIA, NATIONAL INSTITUTE ON AGINGAs toddlers’ brains develop, they trim back the excess synapses among neurons, a process that continues through adolescence. Previous studies have suggested that synapse structure and density might be abnormal in people with autism and in animal models of the disorder.

A study published this month (August 14) in Neuron finds a link between autism and defects in synaptic pruning in humans, and also demonstrates that repairing broken pruning and autophagy mechanisms can improve autism symptoms in a mouse model.

“We were able to treat mice after the disease had appeared,” David Sulzer, a neurobiologist at Columbia University Medical Center who led the study, told The Washington Post.

Specifically, Sulzer’s team treated the mice with rapamycin, an immunosuppressant that inhibits the protein mTOR. The researchers showed that an overactivation of mTOR is responsible for the poor synaptic pruning in the mouse model. “They could treat with rapamycin and restore behavior and restore the pruning,” Kimberly Huber, a neuroscientist at the University of Texas Southwestern Medical Center ...

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  • kerry grens

    Kerry served as The Scientist’s news director until 2021. Before joining The Scientist in 2013, she was a stringer for Reuters Health, the senior health and science reporter at WHYY in Philadelphia, and the health and science reporter at New Hampshire Public Radio. Kerry got her start in journalism as a AAAS Mass Media fellow at KUNC in Colorado. She has a master’s in biological sciences from Stanford University and a biology degree from Loyola University Chicago.

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