Zhiping Mi, MD, MS

Research Assistant Professor of Neurology

Biographical Sketch

Dr. Mi's research interests include neuronal cell death and survival mechanisms in stroke, traumatic brain injury and neurodegenerative diseases. Her current research focus on the role of UCHL1 in traumatic and ischemic brain injury and recovery. The goal of these studies is to develop novel therapeutic interventions that promote gray and white matter preservation and functional recovery in brain injury and neurodegenerative diseases.

Education & Training

  • MD, Shanxi Medical University
  • PhD (candidate), Shanxi Medical University
  • Joint PhD program, Oxford University
  • MS, University of Pittsburgh
  • Post-Doctorate, University of Pittsburgh, University College of London, University of Rochester

Specialized Areas of Clinical, Research and/or Education Interests

Research: Ubiquitin proteasome pathway, oxidative stress, reactive lipid species, cerebral ischemia, traumatic brain injury, Alzheimer’s diseases, neuronal repair and recovery

Professional Organization Membership

  • Society for Neuroscience
  • International Society for Cerebral Blood Flow & Metabolism

Honors & Awards

  • Outstanding Research Award, Zhang Xi-Jun Foundation, Chinese Association of Physiological Science
  • Excellent Medical Student Award, Shanxi Medical University

Selected Recent Publications

Mi Z, Halfter W, Abrahamson EE, Klunk WE, Mathis CA, Mufson EJ, Ikonomovic MD. Tenascin-C Is Associated with Cored Amyloid-beta Plaques in Alzheimer Disease and Pathology Burdened Cognitively Normal Elderly. Journal of neuropathology and experimental neurology. 2016;75 (9):868-76.

Mi Z, Abrahamson EE, Ryu AY, Fish KN, Sweet RA, Mufson EJ, Ikonomovic MD. Loss of precuneus dendritic spines immunopositive for spinophilin is related to cognitive impairment in early Alzheimer's disease. Neurobiol Aging. 2017;55:159-166.

Mi Z, Liu H, Rose ME, Ma J, Reay DP, Ma X, Henchir JJ, Dixon CE, Graham SH. Mutation of a Ubiquitin Carboxy Terminal Hydrolase L1 Lipid Binding Site Alleviates Cell Death, Axonal Injury, and Behavioral Deficits After Traumatic Brain Injury in Mice. Neuroscience. 2021;475 (1):127-136.

Mi Z, Graham SH. Role of UCHL1 in the pathogenesis of neurodegenerative diseases and brain injury. Ageing Res Rev. 2023; 86:101856. doi: 10.1016/j.arr.2023.101856.

Mi Z, Abrahamson EE, Ryu AY, Malek-Ahmadi M, Kofler JK, Fish KN, Sweet RA, Villemagne VL, Schneider JA, Mufson EJ, Ikonomovic MD. Vesicular Glutamate Transporter Changes in the Cortical Default Mode Network During the Clinical and Pathological Progression of Alzheimer's Disease. J Alzheimers Dis. 2023;94(1):227-246.

Mi Z, Povysheva N, Rose ME, Ma J, Zeh DJ, Harikumar N, Bhuiyan MIH, Graham SH. Abolishing UCHL1's hydrolase activity exacerbates ischemia-induced axonal injury and functional deficits in mice. J Cereb Blood Flow Metab 2024:271678X241258809. DOI: 10.1177/0271678X241258809

Mi Z, Ma J, Zeh DJ, Rose ME, Henchir JJ, Liu H, Ma X, Cao G, Dixon CE, Graham SH. Systemic treatment with ubiquitin carboxy terminal hydrolase L1 TAT protein ameliorates axonal injury and reduces functional deficits after traumatic brain injury in mice. Exp Neurol 2024; 373:114650.