Congratulations to the 2026 NFXF Summer Scholar Recipients

The National Fragile X Foundation is proud to expand the 2026 Randi J. Hagerman Summer Scholar Research Awards, this year providing four student researchers with grants of up to $5,000 each to support innovative Fragile X research projects.

Help us in congratulating this year’s awardees: Erin Burnett, Iris Chen, Nura Salem, and Tim Smith — they are helping shape the future of Fragile X research!

The awards are designed to introduce undergraduate and graduate students to the field of Fragile X research. We do this by funding summer projects that meaningfully expand the body of knowledge on Fragile X. These awards help cultivate the next generation of Fragile X researchers while advancing discoveries that benefit our community.

Project Summary: Fragile-X Associated Tremor and Ataxia Syndrome (FXTAS) is not completely understood. For example, we know that some neurodegenerative diseases are known to have disruptions in their blood-brain barrier (BBB), but it’s unknown whether or not FXTAS is included in this. We also know that the BBB is a critical checkpoint in the brain and has components such as proteins and specific cell types that guard access from the bloodstream to the brain. Research has shown that astrocytes – the cell type that makes up the last defense of the BBB – degenerate in FXTAS, but the extent of damage done to the BBB as a whole is unknown.

My goal is to expand our current knowledge by quantifying this data in FXTAS using a technique called immunohistochemistry (IHC). I will visualize proteins that have the potential to travel into the brain when there is weakening of the BBB. This study has potential for not only improved diagnostic methods, but also better therapeutic approaches.

Project Summary: Fragile X-associated tremor/ataxia syndrome (FXTAS) is a neurodegenerative condition that can lead to locomotor, cognitive, and metabolic deficits. There are currently no disease-altering treatments to slow or prevent disease progression. Our project investigates the potential of Semaglutide, an FDA-approved drug commonly used to treat Type 2 Diabetes, in reducing neurodegeneration and improving symptoms in FXTAS patients.

A FXTAS mouse model that mimics key features of the condition will be treated with semaglutide. Histopathology, molecular, and functional assays will be conducted to assess the efficacy of the treatment. Progress in this project could potentially lead to a promising and accessible treatment option for individuals and families affected by FXTAS.

Project Summary: Fragile X Syndrome is caused by mutations in a gene called FMR1, which normally helps neurons communicate and develop properly. Many new treatments aim to replace or fix this gene, but current approaches might not fully copy how the gene is naturally controlled in the body.

Our project looks at specific regions of the gene (untranslated regions) that help regulate when and how the gene is used in neurons. We are testing how these regions affect gene activity and neuron function, especially when cells are stimulated in different ways. By better understanding these parts of the gene, we hope to improve future gene therapies, so they work more effectively and safely for individuals with Fragile X Syndrome.

Project Summary: Fragile X Syndrome happens when a gene called FMR1 is turned off, which changes how brain cells regulate important processes needed for communication and normal function.

In this project, I will use a human brain tissue model of Fragile X Syndrome and help validate genes that change when FMR1 is reduced, using both computer-based analysis and laboratory techniques. I will also begin comparing these changes with those seen in other neurodevelopmental disorders to understand which features are specific to Fragile X syndrome and which may reflect broader shared mechanisms. This research will improve our understanding of Fragile X biology and support the development of better disease models and future treatments.