Xiaoning Bi, PhD, MD
Professor of Physiology
College of Osteopathic Medicine of the Pacific
Phone: 909-469-5487 | Join year: 2006
Ph.D., Neurobiology, Neuroscience Program, University of Southern California, Los Angeles, CA, 1996
M.D., Neuroanatomy, Brain Research Institute, Zurich University, Switzerland, 1994
M.S., Neurophysiology, Third Military Medical University, P.R. China, 1986
M.D., Medicine, Binzhou Medical University, P.R. China, 1982
Postdoctoral Fellow, Dept. of Anatomy and Neurobiology, UCI, Irvine, CA, 1997-1998
Postdoctoral Fellow, Neuroscience, University of Southern California, Los Angeles, CA, 1996-1997
Professor, Department of Basic Medical Sciences, COMP/Western University of Health Sciences, 2012-present
Associate Professor, Department of Basic Medical Sciences, COMP/Western University of Health Sciences, 2006-2012
Assistant Professor In-Residence, Department of Psychiatry and Human Behavior, UCI, Irvine, CA, 2002-2005
Adjunct Assistant Professor, Anatomy and Neurobiology, UCI, Irvine, CA, 1998-2001
Endocrine System; Physiology (COMP)
Gastrointestinal system; Physiology (COMP)
Molecular and Cellular Basis of Life (GCBS)
Molecular and Cellular Basis of Medicine (COMP)
Neuroscience System; Physiology (COMP)
Research in my laboratory seeks to understand how neurons develop, mature, and function properly and how they die when challenged by natural aging process, by intrinsic genetic defects, or by various insults. We hope that by understanding the basic molecular and cellular mechanisms that govern these processes we can develop better preventive and therapeutic strategies for central nervous system disorders in children as well as in elders.
Current Research Projects:
1. Protein homeostasis in synaptic plasticity.
Protein synthesis and degradation in dendritic spines are critically involved in learning and memory. Local protein synthesis can be regulated by multiple factors. This project focuses on neurotrophic factor- and positive AMPA receptor modulator-induced dendritic protein synthesis in synaptic plasticity and spine morphogenesis, as well as the implication of these processes in learning and memory. This project will also test ubiquitination-mediated protein degradation, especially by the E3 ligase, UBE3A (a.k.a. E6-AP), in spine plasticity. Finally, the project will test how deletion of UBE3A results in impairment in learning and memory and in motor function. We hope that results from these studies will help us to better understand neurodevelopmental disorders, such as Angelman syndrome and autism spectrum disorders.
2. Autophagic/lysosomal dysfunction in Niemann-Pick Type C disease and Alzheimer's disease.
Niemann-Pick Type C (NPC) disease is a rare and fatal neurovisceral storage disorder, which currently has no effective treatment. NPC is caused by mutations in NCP1 and NPC2 genes, which encode proteins participating in intracellular cholesterol transport. The pathological hallmark of NPC is accumulation of cholesterol and other lipids in the endosomal-lysosomal systems. Neurodegeneration is a common feature of the disease, and in most cases, is the final cause of death. The mechanisms underlying neurodegeneration are currently unknown; however, accumulating evidence indicates that NPC may share some common pathological mechanisms with Alzheimer's disease (AD). We have found that both diseases have abnormal autophagic activity and lysosomal dysfunction. Both diseases show neurofibrillary tangles and inflammation. Current research on this project focuses on further understanding of how interruption of cholesterol homeostasis leads to neuronal death and on developing strategies to promote NPC neuronal survival. Since NPC and AD share common features neuropathology, we hope our research can also lead to better therapy for AD.
- Baudry M; Zhu G; Liu Y; Wang Y; Briz V; Bi X. (2014) Multiple cellular cascades participate in long-term potentiation and in hippocampus-dependent learning. Brain Res. pii: S0006-8993(14)01617-5.
- Baudry M. and Bi X. (2014) Calcium and signal transduction. (2014) In “Encyclopedia of Neuroscience”. Squire, L. (ed). Elsevier Science, Ltd. Clin Anat. 2014 Jan;27(1):118-30. doi: 10.1002/ca.22340.
- Wang, Y., Zhu, G., Briz, V., Hsu, T.-T., Bi, X., and Baudry M. (2014) A molecular brake controls the magnitude of long-term potentiation. Nature Comm 2014 Jan 7;5:3051. doi: 10.1038/ncomms4051.
- Baudry, M., Bi, X. (2013) Learning and memory: An emergent property of cell motility. Neurobiol Learn Mem. 2013 May 21;104C:64-72.
- Briz, V., Hsu, Y.-T., Li, Y., Lee, E., Bi, X., and Baudry, M (2013) Calpain-2-mediated PTEN degradation contributes to BDNF-induced stimulation of dendritic protein synthesis. J. Neurosci. 2013 Mar 6;33(10):4317-28.
- Baudry, M., Chou, M.M., and Bi, X. (2013) Targeting calpain in synaptic plasticity. Expert Opin Ther Targets. 2013 May;17(5):579-92.
- Baudry, M., Bi, X., and Aguirr, C. (2013) Progesterone-estrogen interactions in synaptic plasticity and neuroprotection. Neuroscience. 2013 Jun 3;239:280-94. 2012 Nov 7.
- Allyson J, Bi X, Baudry M, Massicotte G. (2012) Maintenance of synaptic stability requires calcium-independent phospholipase a(2) activity. Neural Plast. 2012;2012:569149.
- Baudry M, Kramar E, Xu X, Zadran H, Moreno S, Lynch G, Gall C, Bi X. (2012) Ampakines promote spine actin polymerization, long-term potentiation, and learning in a mouse model of Angelman syndrome. Neurobiol Dis. 2012 Aug;47(2):210-5.
- Clausen A, Xu X, Bi X, Baudry M. (2012) Effects of the superoxide dismutase/catalase mimetic EUK-207 in a mouse model of Alzheimer's disease: protection against and interruption of progression of amyloid and tau pathology and cognitive decline. J Alzheimers Dis. 2012 Jan 1;30(1):183-208.
- Qin Q, Liao G, Baudry M, Bi X. Role of calpain-mediated p53 truncation in semaphorin 3A-induced axonal growth regulation. Proc Natl Acad Sci U S A. 2010 Aug 3;107(31):13883-7.
Click link for additional articles: