Our understanding of the neurobiological bases of stuttering remains limited, hampering development of effective treatments that are informed by basic science. Stuttering affects more than 5% of all preschool-age children and remains chronic in approximately 1% of adults worldwide. As a condition that affects a most fundamental human ability to engage in fluid and spontaneous verbal communication, stuttering can have substantial psychosocial, occupational, and educational impacts on those who are affected. This article summarizes invited talks and breakout sessions that were held in June 2023 as part of a 2-day workshop sponsored by the US National Institute on Deafness and Other Communication Disorders. The workshop encompassed topics including neurobiology, genetics, speech motor control, cognitive, social, and emotional impacts, and intervention. Updates on current research in these areas were summarized by each speaker, and critical gaps and priorities for future research were raised, and then discussed by participants. Research talks were followed by smaller, moderated breakout sessions intended to elicit diverse perspectives, including on the matter of defining therapeutic targets for stuttering. A major concern that emerged following participant discussion was whether priorities for treatment in older children and adults should focus on targeting core speech symptoms of stuttering, or on embracing effective communication regardless of whether the speaker exhibits overt stuttering. This article concludes with accumulated convergent points endorsed by most attendees on research and clinical priorities that may lead to breakthroughs with substantial potential to contribute to bettering the lives of those living with this complex speech disorder.

Developmental stuttering is a childhood onset neurodevelopmental disorder with an unclear etiology. Subtle changes in brain structure and function are present in both children and adults who stutter. It is a highly heritable disorder, and 12–20% of stuttering cases may carry a mutation in one of four genes involved in intracellular trafficking. To better understand the relationship between genetics and neuroanatomical changes, we used gene expression data from the Allen Institute for Brain Science and voxel-based morphometry to investigate the spatial correspondence between gene expression patterns and differences in gray matter volume between children with persistent stuttering ( n = 26, and 87 scans) and their fluent peers ( n = 44, and 139 scans). We found that the expression patterns of two stuttering-related genes ( GNPTG and NAGPA ) from the Allen Institute data exhibited a strong positive spatial correlation with the magnitude of between-group gray matter volume differences. Additional gene set enrichment analyses revealed that genes whose expression was highly correlated with the gray matter volume differences were enriched for glycolysis and oxidative metabolism in mitochondria. Because our current study did not examine the participants’ genomes, these results cannot establish the direct association between genetic mutations and gray matter volume differences in stuttering. However, our results support further study of the involvement of lysosomal enzyme targeting genes, as well as energy metabolism in stuttering. Future studies assessing variations of these genes in the participants’ genomes may lead to increased understanding of the biological mechanisms of the observed spatial relationship between gene expression and gray matter volume.