MIT neuroscientists have figured out how the brain is able to focus on a single voice among a cacophony of many voices, shedding light on a longstanding neuroscientific phenomenon known as the cocktail party problem.

This attentional focus becomes necessary when you’re in any crowded environment, such as a cocktail party, with many conversations going on at once. Somehow, your brain is able to follow the voice of the person you’re talking to, despite all the other voices that you’re hearing in the background.

Using a computational model of the auditory system, the team found that amplifying the activity of the neural processing units that respond to features of a target voice, such as its pitch, allows that voice to be boosted to the forefront of attention.

“That simple motif is enough to cause much of the phenotype of human auditory attention to emerge, and the model ends up reproducing a very wide range of human attentional behaviors for sound,” says Josh McDermott, a professor of brain and cognitive sciences at MIT, a member of MIT’s McGovern Institute for Brain Research and Center for Brains, Minds, and Machines, and the senior author of the study.

MIT researchers have discovered that two common genetic mutations that cause Rett syndrome each set off a molecular chain of events that compromises the structural integrity of developing brain blood vessels, making them leaky. The study traces the problem to overexpression of a particular microRNA (miRNA-126-3p), and shows that tamping down the miRNA’s levels helps to rescue the vascular defect.

Rett syndrome is a severe developmental disorder affecting both the brain and body. It is caused by various mutations in the widely expressed MECP2 gene, but the first symptoms don’t become apparent until affected children (mostly girls) reach 2-3 years of age. Because that’s a critical time in development for the brain’s blood vessels, neuroscientists in The Picower Institute for Learning and Memory at MIT embarked on a study to model how two common but distinct MeCP2 mutations may affect vascular development and contribute to the disease’s profound neurological pathology.

To conduct the research published recently in Molecular Psychiatry, lead author Tatsuya Osaki and senior author Mriganka Sur developed advanced human tissue cultures to model vessel development, with and without the MeCP2 mutations. The cultures not only enabled them to model and closely observe how the mutations affected the vessels, but also allowed them to molecularly dissect the problems they observed and then to test an intervention that helped.

MIT Picower Professor Li-Huei Tsai, who has led The Picower Institute for Learning and Memory since 2009, will step down from the role of director at the end of the academic year in May. Her decision frees her to focus exclusively on her academic work, including her continued leadership of MIT’s Aging Brain Initiative and the Alana Down Syndrome Center. Meanwhile, the search for the Picower Institute’s next director has begun.

“During her exceptional 16-year tenure in the role of director, Li-Huei has led substantial growth at the Picower Institute,” says Nergis Mavalvala, dean of the MIT School of Science and the Curtis and Kathleen Marble professor of astrophysics. “She has markedly expanded the faculty — eight of the current 16 labs joined Picower under her directorship — through successful recruitment of highly talented neuroscientists. She has done this, and more, all while leading one of our most productive and influential labs, working on a quintessentially grand challenge in human health: combating Alzheimer’s disease.”