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.
Xinyu Zhao
Xinyu Zhao, PhD – Slide of the Week
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.
Xinyu Zhao, PhD – Slide of the Week
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), …
Improved technique illuminates fragile X protein
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.
Xinyu Zhao, PhD – Slide of the Week
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.
Cell component breakdown suggests possible treatment for multiple neural disorders
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.
Connecting research and clinics to help those with autism
One of the goals of the study is to discover how genetic variations in young people with ASD are related to brain changes that lead to clinical symptoms of the disorder, such as impaired social interaction and repetitive behaviors.
“If you think about it, in between genes and clinical symptoms [of ASD] are changes in brain development,” says Lainhart. “Genes first impact brain development, and as a result of changes in how the brain develops, there are clinical manifestations of what we recognize as ASD.”
Xinyu Zhao, PhD – Slide of the Week
Adult neural stem cells in mouse models of fragile X syndrome (FXS) have elevated histone acetylation, leading to reduced neurogenesis. Treatment with either Nutlin-3 or Curcumin rebalances histone acetylation and rescues cognitive functions
Xinyu Zhao receives 2018 National Fragile X Foundation (NFXF) Research Award
Xinyu Zhao, PhD, received the 2018 National Fragile X Foundation (NFXF) Research Award for outstanding contributions to the understanding of fragile X syndrome. Zhao is a professor of neuroscience and Waisman Center investigator at the University of Wisconsin-Madison.
Study points researchers toward new therapies for fragile X syndrome
By Adityarup “Rup” Chakravorty New insights into the molecular machinations behind fragile X syndrome, the most common inherited intellectual disability, may help researchers develop potential therapies. Fragile X is a genetic condition that affects one …