Dr. Guilian Xu
Research Assistant Scientist, Neuroscience
Post Doc, Neuropatholgy, Johns Hopkns University, 2001-2005
Ph.D., Physiology, The University of Hong Kong, 2001
B.S., Biochemistry, Sichuan University, China 1991
Contact Dr. Xu
Research Focus and Aims
Different kind of neurodegenerative disorders, including Alzheimer’s disease, amyotrophic lateral sclerosis (ALS), and Huntington’s disease, all share the similar pathologic feature that misfolded protein aggregates in the central neuronal system. It has been proposed that they may share similar mechanisms of pathogenesis, although for now no single common mechanism has yet emerged. The familiar forms of these diseases can be modeled by transgenic mouse models. I am focus on investigating the mechanisms of the effect of these misfolded proteins on the protein homeostasis using proteomics and systematic biology strategies. This work involves the use of transgenic mouse models, human tissues, and cell culture systems to examine the soluble, insoluble proteins and their relationship with some bioinformatics tools.
Current Research Projects
- Proteomics and systemic biology study on proteostasis of AD, HD and ALS transgenic mouse models
- The role of LRP on amyloid deposition on transgenic mouse model
- Amyloid clearance and senile plaque dynamic study on tetracycline inducible transgenic mouse model of Alzheimer’s disease
- Developing inducible stable cell lines expressing YFP fused SOD1 for ALS drug screening
- Characterize transgenic mice overexpressing mutant or wildtype human SOD1
- Tebbenkamp AT, Green C, Xu G, Denovan-Wright EM, Rising AC, Fromholt SE, Slunt HH, Swing D, Mandel RJ, Tessarollo L, Borchelt DR. Transgenic mice expressing caspase-6 derived N-terminal fragments of mutant huntingtin develop neurologic abnormalities with predominant cytoplasmic inclusion pathology composed largely of a smaller proteolytic derivative. Hum Mol Genet. 2011 Apr 22.
- Xu G, Karch C, Li N, Lin N, Fromholt D, Gonzales V, Borchelt DR. Receptor-associated protein (RAP) plays a central role in modulating Abeta deposition in APP/PS1 transgenic mice. PLoS One. 2008 Sep 8;3(9):e3159.
- Wang J, Xu G, Li H, Gonzales V, Fromholt D, Karch C, Copeland NG, Jenkins NA, Borchelt DR. Somatodendritic accumulation of misfolded SOD1-L126Z in motor neurons mediates degeneration: alphaB-crystallin modulates aggregation. Hum Mol Genet. 2005 Aug 15;14(16):2335-47.
- Savonenko A, Xu GM, Melnikova T, Morton JL, Gonzales V, Wong MP, Price DL, Tang F, Markowska AL, Borchelt DR. Episodic-like memory deficits in the APPswe/PS1dE9 mouse model of Alzheimer’s disease: relationships to beta-amyloid deposition and neurotransmitter abnormalities. Neurobiol Dis. 2005 Apr;18(3):602-17.
- Sheng JG, Bora SH, Xu G, Borchelt DR, Price DL, Koliatsos VE. Lipopolysaccharide-induced-neuroinflammation increases intracellular accumulation of amyloid precursor protein and amyloid beta peptide in APPswe transgenic mice. Neurobiol Dis. 2003 Oct;14(1):133-45.
- Xu G, Gonzales V, Borchelt DR. Abeta deposition does not cause the aggregation of endogenous tau in transgenic mice. Alzheimer Dis Assoc Disord. 2002 Jul-Sep;16(3):196-201.
- Xu G, Gonzales V, Borchelt DR. Rapid detection of protein aggregates in the brains of Alzheimer patients and transgenic mouse models of amyloidosis. Alzheimer Dis Assoc Disord. 2002 Jul-Sep;16(3):191-5.
- Lesuisse C, Xu G, Anderson J, Wong M, Jankowsky J, Holtz G, Gonzalez V, Wong PC, Price DL, Tang F, Wagner S, Borchelt DR. Hyper-expression of human apolipoprotein E4 in astroglia and neurons does not enhance amyloid deposition in transgenic mice. Hum Mol Genet. 2001 Oct 15;10(22):2525-37.
- Tang F, Li H, Nag S, Xu G, Chan T. Transgenic mouse and chemical lesion approaches to the study of Alzheimer’s disease. Chin Med J (Engl). 1997 Aug;110(8):642-7. Review.