 Dr. Xiaoning Bi--Associate Professor of Physiology
| Background |
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1982 M.D: Medicine,
Binzhou Medical University, P.R.C |
| 1982-1983 Instructor, Binzhou Medical College, P.R.C. |
1983-1986 M.S.: Physiology,
Third Medical University of PLA, P.R.C. |
1991-1994 M.D.: Research Assistant/MD Student;
Brain Research Institute, Zurich University,
Switzerland
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1996 Ph.D.: Neurobiology, Neuroscience,
University of Southern California,
Los Angeles, CA |
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1996-1997 Postdoctoral Fellow, Neuroscience,
University of Southern California,
Los Angeles, CA |
1997-1998 Postdoctoral Fellow,
Department of Anatomy and Neurobiology,
UCI, Irvine, CA |
1998-2001 Adjunct Assistant Professor,
Anatomy and Neurobiology, UCI,
Irvine, CA |
2002-2005 Assistant Professor In-residence,
Department of Psychiatry and
Human Behavior, UCI,
Irvine, CA |
2005-Present Associate Professor,
Department of Basic Medical Sciences,
Western University of Health Sciences,
College of Osteopathic Medicine of the Pacific |
Date Started with Western University & College of Osteopathic Medicine of the Pacific
November 2005
Current Course Listing: |
| Dr. Bi's main training has been in the field of physiology and neurobiology and will be teaching the core physiology course involving neurophysiology. |
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Selected Publications:
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Bi, X., Liu J., Yao Y., Baudry M., and Lynch G. (2005) Deregulation of GSK-3ß and NF- B is associated with neurodegeneration in Npc1-/- mouse brain. Am J Pathol (in press).
Lin, B., Kramar, E., Bi, X., Brucher, F., Gall, C.M., and Lynch, G. (2005) Theta stimulation polymerizes actin in dendritic spines of hippocampus. J. Neurosci. 25(8):2062-2069.
Bi, X., Baudry M., Liu J., Fu L., Yao Y., Brucher F., and Lynch G. (2004) Inhibition of geranylgeranylation mediates the effects of HMG-CoA reductase inhibitors on microglia. J. Biol. Chem. 279(46):48238-45, Epub 2004 Sep 9.
Baudry, M., Yao , Y., Simmons, D., Liu, J., and Bi, X. (2003) Postnatal development of inflammation in a murine model of Niemann-Pick disease type C: immunohistochemical observations of microglia and astroglia. Exp. Neurol. 184:887-903.
Lynch, G. and Bi, X. (2003). Lysosomes and brain aging in the mammals. Neurochemical Research. Vol 28, No 11, 1725-1734.
Bi, X., Yong, A.P., Zhou, J., Ribak, C.E., Lynch, G. (2001) Rapid induction of intraneuronal neurofibrillary tangles in apolipoprotein E-deficient mice. Proc Natl Acad Sci U S A. 98(15): 8832-8837.
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| Reserch Interests: |
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Dr. Bi's primary research interest consists of
- understanding cellular and molecular mechanisms of synaptic plasticity and of neurodegeneration
- based on the knowledge seeking novel therapies for disorders of the central nervous system (CNS).
Currently, the laboratory has the following primary research areas
- Studying the role of cell adhesion protein integrin and cytoskeletal protein actin in synaptic plasticity (a collaborative project with Drs. Gary Lynch and Christine Gall at UCI)
- Investigating the roles of endosomes/lysosomes and autophagy in brain ageing and age-related neurodegeneration,
- Seeking novel molecular and cellular therapies to limit neurodegeneration and to promote regeneration and neurogenesis. Ongoing projects are:
Project One: Actin polymerization in synaptic plasticity and the roles of integrin (a collaborative project with Drs. Gary Lynch and Christine Gall at UCI).
Using a recently introduced method for labeling F-(polymerized) actin in hippocampal slices, they found that the theta burst stimulation conventionally employed to induce LTP (long-term potentiation) caused rapid and persistent polymerization of actin in a subpopulation of spines corresponding in number (and location) to the potentiated population of synapses. These effects were completely blocked by manipulations that disrupt the formation of LTP. Currently, they are testing the hypothesis that actin polymerization is driven by adhesion molecule integrin.
Project Two: Endosomal/lysosomal dysfunction in brain aging, neurodegeneration, and inflammation
Endosomal-lysosomal dysfunction, including altered endocytosis and intracellular protein trafficking and changes in levels of endosomal/lysosomal enzymes, has been demonstrated as the earliest pathology in brains with Alzheimer's disease (AD). Lysosomal proteases are involved in generation of the toxic amyloid beta peptide and truncation of tau, two processes critically linked to the pathological hallmarks of the diseases: amyloid plaques and neurofibrillary tangles. They have obtained evidence that lysosomal dysfunction in diverse mammalian animals appears early in adulthood in brain areas known to be particular vulnerable to age-related neurodegenerative diseases. Our in vitro studies have showed that experimentally-induced lysosomal dysfunction in cultured brain slices triggers a wide array of changes associated with the aged human brain, including lysosomal proliferation and formation of neurofibrillary tangles. Currently, they are using transgenic mice and tissue culture models to determine the consequences of endosomal-lysosomal dysfunction on processing of AD-related proteins, cell signal transduction, and cell death pathways in neurons. We are also studying the consequences of endosomal-lysosomal dysfunction on the function of various glial cells.
Project Three: Neuroprotection and circuitry rewiring: Effects of trophic factors and stem cells
The third focus of the laboratory is to seek routes of rebuilding neuronal circuits through facilitating axonal regeneration, dendrites and spine reconstruction, and neurogenesis. They are interested in testing whether neurotrophic factors, such as BDNF, protect neurons against lysosomal dysfunction induced neurodegeneration in our cultured hippocampal models prepared from different transgenic mice. They are also interested in seeking molecular and cellular vehicles that promote axonal regeneration after acute injury in cultured hippocampal slices prepared from transgenic mice expressing YFP proteins. Finally, we are interested in testing neurogenesis in dentate gyrus after acute and chronic injuries, and transplantation of stem cells in cultured hippocampal slice as well as in vivo. Human and murine embryonic and neural stem cells will be used and conditions for stem cell differentiation and survival will be developed and optimized. Our experimental approaches include real-time morphological imaging in living tissues prepared from genetically engineered mice, intracellular biochemical fluorescent imaging, lysosomal and mitochondrial imaging, confocal fluorescent microscopy, signaling transduction analyses, electrophysiology and molecular biology.
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Publications:
Book: |
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Baudry, M., Bi X., and Schreiber S.S (2005) Synaptic Plasticity: Basic Mechanisms to Clinical Applications. Series: Neurological Disease and Therapy. Marcel Dekker, New York
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| Book Chapters: |
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Bi X. (2005) Lysosomal dysfunction in brain aging and neurodegeneration: roles in trophic signaling and neuroinflammation. In "Synaptic Plasticity: Basic Mechanisms to Clinical Applications. Series: Neurological Disease and Therapy". Baudry, M., Bi X., and Schreiber S.S. (eds). Marcel Dekker, New York , pp53-74.
Bi X. and Baudry M. (2000) Neurotransmitters and receptors. In "The Treatment of Epilepsy: Principles and Practice". 3rd edition. E. Wyllie (ed.). Lippincott Williams & Wilkins, Baltimore, MD.
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