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 reviewed literature from 2010 to 2023 on social communication in individuals with Neurofibromatosis type 1 (NF1) and Noonan syndrome (NS). Our summary emphasizes the links between specific genes associated with these syndromes and their impact on social communication abilities. We found that specific molecular and neural mechanisms, including GABAergic transmission, serotonin, dopamine, and glia and white matter connectivity, play a significant role in social communication in individuals with NF1 and NS. Furthermore, we identified that brain regions commonly associated with attention and memory, such as the hippocampus and striatum, may play an important role in social communication in these populations.
Sanchez et al., 2024
Our analysis showed that both Neurofibromatosis type 1 (NF1) and Noonan syndrome (NS) significantly impact the integrity of white matter in children's brains. These findings suggest that the Ras–MAPK pathway is crucial for white matter development in this population. Although we observed distinct patterns in how each syndrome affects white matter integrity, we also noted significant similarities in the social challenges encountered by children with NF1 and NS.
Sanchez et al., 2024
Our analysis revealed that children with RASopathies exhibit significant differences in cortical surface area compared to typically developing children. In particular, children with Noonan syndrome and Neurofibromatosis type 1 showed reduced surface area in the occipital regions of the brain.
McGhee et al., 2024
Photo Gallery
Holiday Brunch!
Lab Talks
Git Workshop
Tamar's Session at the 5th International Annual Rasopathies Network Symposium!
An evening for the RASopathies community
2024 Plant Exchange
A BRIDGE Webinar!
Farewell to Monica!
Yaffa Presenting at ISBP 2023
Lunch in Dr. Green's backyard
2024 Summer Student Presentations
Poster Session with Jen
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Outing with the Lab!
Marin Headland Hike
Thanksgiving Celebrations and Team Coffee
