Dr. Weiping Qin’s research focuses on developing innovative therapeutic strategies to prevent and reverse skeletal and neurological impairments associated with spinal cord injury (SCI). His laboratory investigates the molecular and cellular mechanisms underlying bone loss, muscle atrophy, and neurodegeneration following SCI, with the goal of identifying novel molecular targets for treatment. Dr. Qin’s work integrates approaches from molecular biology, neuroscience, and regenerative medicine to elucidate how injury-induced changes in signaling pathways, inflammation, and oxidative stress contribute to tissue degeneration. He also explores pharmacological and biological interventions that may enhance neural repair, bone regeneration, and functional recovery. Through translational studies, his team aims to bridge fundamental discoveries with clinical applications, advancing potential therapies to improve quality of life and outcomes for patients with SCI. His research has been recognized for its contributions to understanding neurodegenerative and skeletal pathology, and for identifying key therapeutic avenues to promote tissue protection and regeneration.
Featured Publications:
Qin, W., Ho, L., Pompl, P. N., Xiang, Z., Wang, J., Zhao, Z., Peng, Y., Cambareri, G., & others. (2004). Diet-induced insulin resistance promotes amyloidosis in a transgenic mouse model of Alzheimer’s disease. The FASEB Journal, 18(7), 902–904.
Qin, W., Yang, T., Ho, L., Zhao, Z., Wang, J., Chen, L., Zhao, W., Thiyagarajan, M., & others. (2006). Neuronal SIRT1 activation as a novel mechanism underlying the prevention of Alzheimer disease amyloid neuropathology by calorie restriction. Journal of Biological Chemistry, 281(31), 21745–21754.
Qin, W., Haroutunian, V., Katsel, P., Cardozo, C. P., Ho, L., Buxbaum, J. D., & others. (2009). PGC-1α expression decreases in the Alzheimer disease brain as a function of dementia. Archives of Neurology, 66(3), 352–361.
Wang, J., Ho, L., Qin, W., Rocher, A. B., Seror, I., Humala, N., Maniar, K., Dolios, G., & others. (2005). Caloric restriction attenuates β-amyloid neuropathology in a mouse model of Alzheimer’s disease. The FASEB Journal, 19(6), 1–18.
Yamashita, T., Kaneko, S., Shirota, Y., Qin, W., Nomura, T., Kobayashi, K., & others. (1998). RNA-dependent RNA polymerase activity of the soluble recombinant hepatitis C virus NS5B protein truncated at the C-terminal region. Journal of Biological Chemistry, 273(25), 15479–15486.
Shirota, Y., Luo, H., Qin, W., Kaneko, S., Yamashita, T., Kobayashi, K., & others. (2002). Hepatitis C virus (HCV) NS5A binds RNA-dependent RNA polymerase (RdRP) NS5B and modulates RNA-dependent RNA polymerase activity. Journal of Biological Chemistry, 277(13), 11149–11155.