Advancing knowledge of human development, developmental disabilities, and neurodegenerative diseases.
Research has shown voluntary running is an activity most commonly associated with the reversal of negative impacts of aging and neurodegeneration, but little is understood about why that is.
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.
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.”
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, 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.
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 in 4,000 males and one in 6,000 females. It’s linked to variations in the gene that makes a protein called …
Several Waisman Center investigators played key roles in crafting research proposals that were recently selected as ‘cluster hires’ by the University of Wisconsin–Madison. UW–Madison’s Cluster Hiring Initiative was launched in 1998 as an innovative partnership between the university, state and the Wisconsin Alumni Research Foundation (WARF). According to the UW–Madison Office of the Provost, the …
Integrative Single-Cell Transcriptomics Reveal Molecular Networks Defining Neuronal Maturation during Postnatal Neurogenesis Legend: Left: An illustration of coronal section of Nissl-stained adult mouse brain; Confocal images showing that most of DsRed+ (red) cells in DCX-dsRed mouse brains express immature neuron marker doublecortin (DCX, green). Middle: A schematic of the experimental design for single-cell transcriptome analysis. Right: Enrichment …
