SFARI Research: Highlights from 2016

The Simons Foundation Autism Research Initiative funds more than 350 researchers who carry out groundbreaking research — from building brain cells from scratch to understanding how hypersensitivity to touch may relate to social difficulties.

Mice deficient in the gene Rai1 are characteristically obese with learning, memory and balance problems. In normal adult mice, the gene is widely expressed through the brain (yellow marks regions with higher expression). Image Credit: Liqun Luo Laboratory/Stanford University

The Simons Foundation Autism Research Initiative (SFARI) currently funds more than 350 researchers, known as SFARI Investigators, who carry out groundbreaking autism research across the globe. Their work spans a wide range of subjects — from building brain cells from scratch in the lab to understanding how hypersensitivity to touch may relate to social difficulties. Below are some highlights of SFARI Investigators’ research in 2016.

Reversing Autism Symptoms

A new study suggests that it may be possible to reverse some behavioral traits linked to a particular form of autism as late as adulthood, at least in mice. SFARI Investigator Guoping Feng of the Massachusetts Institute of Technology and his collaborators looked at mice with nonfunctioning copies of SHANK3, an autism risk gene believed to contribute to about 1 percent of all autism cases. They found that these mice can recover from traits such as obsessive grooming and social deficits if the gene gets turned on, even in adulthood.

SHANK3 is one of many genes involved in the formation of synapses, the junctions between neurons that allow them to send signals to each other. In mice lacking SHANK3, neurons in a brain region called the striatum communicate at synapses less effectively than do those of control mice. But turning the gene on in adulthood reverses this deficit and also rescues the mice’s obsessive grooming and social deficits, the researchers reported February 25, 2016, in Nature.

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