7703 Floyd Curl Drive San Antonio, TX 78229

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Shenfeng Qiu, MD, PhD
Professor, Basic Medical Sciences
University of Arizona College of Medicine-Phoenix

Title: "MET receptor tyrosine kinase – from neurodevelopment to neurodegeneration"

Summary: Our laboratory's long-term mission is to understand how genetic risk factors predispose individuals to neurodevelopmental disorders, including autism, by influencing normal brain development and physiological function. Additionally, I am deeply interested in the neurocircuit basis of behavior and the molecular and synaptic mechanisms underlying aging and neurodegeneration. For the past 15 years, a major focus of our lab has been investigating the role of the MET receptor tyrosine kinase, a prominent autism risk factor, in forebrain development. Our research has demonstrated that MET signaling is a critical neural mechanism regulating dendritic spine formation, synaptogenesis, circuit plasticity, and maturation. Furthermore, MET plays a crucial role in mediating the functional and structural adaptation of forebrain circuit functions. This work has been supported by the NIMH through K99/R00/R01 grants. Beyond its neurodevelopmental role, our lab and other studies suggest that MET signaling may be significant in the aging and degenerating brain. Recent findings show that MET protein, heavily expressed in excitatory neurons during early brain development, is reduced in Alzheimer's disease (AD) patients' brains. Moreover, hepatocyte growth factor (HGF), the sole ligand for MET and primarily expressed in astrocytes, is elevated in the cerebrospinal fluid of AD patients and associated with small vessel pathology in AD and dementia. Synapse loss and the degradation of circuit connectivity are common in many neurological conditions, including ischemia, stroke, and traumatic brain injury. Consequently, another central focus of our research is to leverage the HGF-MET duo to enhance synaptogenesis and plasticity in adult brain circuits. This approach aims to combat aging, neurodegeneration, and neurological conditions characterized by synapse loss and cognitive decline. We have submitted several NIH grant proposals to explore these diverse research directions.

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