Reactivating the Fragile X Gene in Young Mice Reverses Symptoms

Reactivating the Fragile X Gene in Young Mice Reverses Symptoms

A new FRAXA-funded research project offers hope that Fragile X syndrome could be treated by reactivating the gene which is shut down in people with the syndrome. Researchers at the University of California, Riverside report that they were able to reduce FXS symptoms by inserting the FMR1 gene into the brains of very young mice.

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Fragile X Mutant Mouse Models

Fragile X Mutant Mouse Models

With $375,000 in grants from the FRAXA Research Foundation since 2009, Dr. David Nelson has developed an impressive array of advanced mouse models of Fragile X, at Baylor College of Medicine. These models are available to investigators worldwide on request. This resource has been essential for a broad, rapid distribution of Fragile X and related gene mouse models and has increased the pace of Fragile X research.

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Researcher David Nelson, PhD, Explores New Cell Strategies for Fragile X Syndrome, FXTAS and FXPOI

Researcher David Nelson, PhD, Explores New Cell Strategies for Fragile X Syndrome, FXTAS and FXPOI

It’s rare to find a researcher working on the Big Three — Fragile X Syndrome (FXS), Fragile X-associated Tremor/Ataxia Syndrome (FXTAS) and Fragile X-associated primary ovarian insufficiency (FXPOI). Then again, David Nelson, PhD, is the rare bird. Nelson is a professor of Molecular and Human Genetics, Baylor College of Medicine, and director of Baylor’s Graduate Program in Integrative Molecular and Biomedical Sciences. He has been involved in FXS research since the late 1980s where he helped identify the mutation and the FMR1 gene. These days, researchers in Nelson’s lab at Baylor are studying FXS, FXTAS and FXPOI using mouse models.

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