Fragile X syndrome, the most common form of inherited intellectual disability, may be unfolding in brain cells even before birth, despite typically going undiagnosed until age 3 or later.
A new study published today in the journal Neuron by researchers at the University of Wisconsin–Madison showed that FMRP, a protein deficient in individuals with fragile X syndrome, has a role in the function of mitochondria, part of a cell that produces energy, during prenatal development. Their results fundamentally change how scientists understand the developmental origins of fragile X syndrome and suggest a potential treatment for brain cells damaged by the dysfunction.
Xinyu Zhao is a neuroscience professor and neurodevelopmental diseases researcher at UW–Madison’s Waisman Center. Four postdoctoral fellows in her lab led the study.
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