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.”

Proposals by Waisman investigators selected for UW-Madison Cluster Hire Initiative

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 …