Xinyu Zhao, PhD, and Anita Bhattacharyya, PhD, will partner on research over the next four years to better understand the molecular underpinnings behind the diversity of FXS symptoms and how that diversity may inform the search for effective therapies.
Since 2016, the Waisman Center has partnered with Lawrence University in Appleton, Wisconsin to provide summer research internships for undergraduate Lawrence students in the labs of Waisman researchers.
Sabrina Huang, a rising senior in the Waisman lab of Xinyu Zhao, PhD, was awarded inaugural support from the endowed Morris H. Aprison Scholar Fund for Undergraduate Research.
Neurodevelopmental impairment contributes to the hallmark cognitive disability in individuals with Down syndrome (DS, trisomy 21, T21).
A newer cancer drug may also be a treatment option for a leading intellectual and developmental disability. Fragile X syndrome (FXS) is the most common form of inherited intellectual disability.
Voluntary running enhances adult hippocampal neurogenesis, with consequences for hippocampal-dependent learning ability and mood regulation. However, the underlying mechanism remains unclear. Here, we show that voluntary running induces unique and dynamic gene expression changes specifically within the adult-born hippocampal neurons, with significant impact on genes involved in neuronal maturation and human diseases. We identify the regulator of G protein signaling 6 (RGS6) as a key factor that mediates running impact on adult-born neurons.
Title: Identification of FMR1-regulated molecular networks in human neurodevelopment Legend: Generation of FMR1-FLAG hPSCs using one-step seamless genome editing using CRISPR-Cas9, Neural differentiation of hPSCs into forebrain dorsal NPCs (dNPC) and ventral MGE-like NPCs (vNPC), …
Researchers at the Waisman Center made a significant step in understanding the function of a specific protein, FMR1, whose absence causes fragile X syndrome, or FXS. Waisman investigators Xinyu Zhao, PhD, and Anita Bhattacharyya, PhD, with research associate Meng Li, published their paper “Identification of FMR1-regulated molecular networks in human neurodevelopment” in the March issue of the journal Genome Research.
Fragile X syndrome results from a loss of the RNA-binding protein fragile X mental retardation protein (FMRP). How FMRP regulates neuronal development and function remains unclear. Here we show that FMRP-deficient immature neurons exhibit impaired dendritic maturation, altered expression of mitochondrial genes, fragmented mitochondria, impaired mitochondrial function, and increased oxidative stress.
UW-Madison research published today (Feb. 11, 2019) reveals how one mutation causes fragile X, the most common inherited intellectual disability. “Fragile X syndrome has been studied as a model of intellectual disability because in theory it’s comparatively simple,” says senior author Xinyu Zhao, a professor of neuroscience in the Waisman Center at the University of Wisconsin–Madison.