Our Vision
The BRIDGE Lab at Stanford is dedicated to researching the effect of altered genetics on brain development and neuropsychiatric conditions, with the aim of improving children’s mental health and development. Our research is focused on identifying the mechanistic targets for medical interventions through clinical research. We are committed to translational research, which provides a deeper understanding of the brain that can ultimately enhance the lives of those affected by neuropsychiatric conditions.
Our Research
The BRIDGE Lab focuses on the genetic and neural mechanisms underlying neurodevelopmental disorders, particularly those associated with RASopathies like Noonan syndrome (NS) and Neurofibromatosis 1 (NF1). We utilize advanced brain imaging, computational modeling, and community-engaged approaches to translate genetic insights into clinical applications.
More specifically, the current projects in our laboratory include:
- Analysis of neural correlates in RASopathies: Investigating the effects of NS-related gene mutations on brain development, particularly in the striatum and whole-brain connectivity.
- Mapping brain networks in NF1: Characterizing structural and functional brain networks in NF1, comparing them to typically developing controls and children with NS.
- Predicting neurodevelopmental disorders incorporating common genetics: Utilizing Polygenic Risk Scores (PRS) to enhance predictions of neurodevelopmental outcomes like ADHD and ASD in high-risk children with RASopathies.
- Improving Care through Community Engagement: Engaging with families affected by RASopathies to identify and address barriers to quality care, particularly in underserved populations.
Overall, our research aims to provide novel insights into the genetic and neural basis of these disorders, driving the development of more precise diagnostic tools and therapeutic strategies.
Findings
We investigated differences in the structure of the cerebellum in youth with Neurofibromatosis type 1 (NF1) compared to unaffected youth. We found that white matter volume in the cerebellum was larger in youth with NF1, and differences in white matter microstructure were also observed. We also implemented a support vector model to better understand which factors (e.g., cerebellum neuroimaging metrics, neurocognitive) contribute most to distinguishing youth with NF1 from unaffected youth and found that the top three weights were white matter volume, ratings of child mobility, and the neurite density index. These may be underlying mechanisms of cerebellum-mediated neurocognitive deficits in NF1 and should be explored further.
Pardej et al., 2026
Our findings indicate that children with Noonan syndrome (NS) and Neurofibromatosis type 1 (NF1) exhibit higher levels of irritability than their typically developing peers. Although overall irritability levels were comparable between the NS and NF1 groups, the pattern of associations with behavioral domains, specifically attention symptoms and social difficulties, differed. In particular, within the NS group, irritability was more strongly linked to social difficulties, suggesting that interventions targeting irritability may help improve social functioning in this population.
Serrur et al., 2025
Our findings reveal that children with PTPN11-associated NS, NSML, and SOS1-associated NS, exhibited significantly elevated scores for autism spectrum disorder-related traits, poorer social functioning, and increased emotional challenges compared to typically developing peers. Notably, individuals with NSML showed heightened attention problems. Additionally, we identified a correlation between SHP2 activation levels, a key signaling protein involved in the RAS-MAPK pathway, and the severity of restricted and repetitive behaviors. These results have clinical relevance, as nearly 30% of individuals with NS and NSML exhibit autism-related behaviors. Understanding these genetic and biological mechanisms can pave the way for more tailored interventions.
McGhee et al., 2026