Guoping Feng is the James and Patricia Poitras Professor in Neuroscience at the McGovern Institute for Brain Research in the Department of Brain and Cognitive Sciences at the Massachusetts Institute of Technology and is a member of the Stanley Center for Psychiatric Research at the Broad Institute.
Yufeng Shen is an assistant professor of systems biology and biomedical informatics at Columbia University. He received his B.S. in biochemistry and molecular biology from Peking University and his Ph.D. in computational biology from Baylor College of Medicine. At Baylor, Shen led the analysis of the first human genome sequenced by next-generation technologies.
Guoping Feng and Michael Halassa create mice with global or thalamic-specific loss of the ASD-risk gene PTCHD1 to show specific roles for thalamic PTCHD1 in ASD-like behaviors.
The neurobiology behind the classic signs of autism — repetitive behaviors, impaired social interactions and language deficits — is largely unknown. Based on their studies on a mouse model of obsessive-compulsive disorder, Guoping Feng and his colleagues at Duke University propose that an imbalance between two circuits of neurons may underlie the repetitive behaviors associated with autism.
Many genes implicated in autism encode proteins at synapses, the connections between neurons. These proteins include the neuroligin-neurexin complex and the PSD95-SAPAP-SHANK complex at synapses that release the neurotransmitter glutamate[ref]Ting J.T. et al. Ann. Rev. Neurosci. 35, 49-71 (2012) PubMed[/ref].
Genetics is important in the etiology of autism, with many identified candidate genes linking autism to synaptic pathology. Although understanding autism at the level of genes and synapses is essential, developing novel therapeutics requires an understanding of the dysfunction of neural circuits that control autism-related behavior. This entails knowledge of the affected neuronal subtypes and how their interactions may be disrupted in distinct brain regions and developmental stages.
Using SHANK3 conditional knock-in mice, Guoping Feng shows that adult re-expression of SHANK3 improves cellular and behavioral abnormalities, including ASD-like deficits.
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