Advancing knowledge of human development, developmental disabilities, and neurodegenerative diseases.
Waisman Center researchers are creating a new approach to study how changes to brain development in the womb result in intellectual disability in people with Down syndrome.
Down syndrome (DS, trisomy 21) is characterized by intellectual impairment at birth and Alzheimer's disease (AD) pathology in middle age. As individuals with DS age, their cognitive functions decline as they develop AD pathology.
The Biden administration’s loosening of restrictions on the use of fetal tissue in research will allow UW-Madison scientists to continue such studies, which opponents have tried several times to ban in Wisconsin.
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.
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.
Neuropathology of the Down syndrome cerebral cortex includes fewer interneurons in upper cortical layers.
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 …
Generation of Human Induced Pluripotent Stem Cells from Unaffected Neonatal Skin Cells - We have generated and characterized iPSC clones from three unaffected, neonatal individuals using non-integrating episomal reprogramming plasmids expressing OCT4, SOX2, LIN28, KLF4, and c-Myc.
Waisman Center researchers Anita Bhattacharyya and Xinyu Zhao are looking to make stem cells glow. That glow will tell them that they have successfully turned on a gene that is usually turned off in individuals with fragile X syndrome. Turning on this gene – called FMR1 – could be an important way to treat this …
Title: Creation of a human reporter stem cell line for detecting fragile X mental retardation (FMR1) gene reactivation in human neural cells. Legend: Fragile X syndrome (FXS) is the most common inherited cause of intellectual disability and a major genetic cause of autism. FXS is caused by mutational trinucleotide expansion in the FMR1 gene leading …
