Xugang Xia, M.D., Ph.D.

Contact Dr. Xia

1020 Locust Street
Jefferson Alumni Hall, Suite 508
Philadelphia, PA 19107

(215) 503-1037

Medical School
M.D. (equivalent), Hunan Medical University, China, 1990

M.S., rehabilitation and physical therapy, Hunan Medical University, China, 1995

Ph.D. (equivalent), Tuebingen University, Germany, 2001

University Appointment
Professor

Research and Clinical Interests
As a medical researcher and educator, I have been trained in medical schools for clinic work and in basic sciences for medical research. My experience in clinical work, as a neurologist, and in basic science, as a neuroscientist, provides me with a unique understanding as to how important medical research is to human health. Using multidisciplinary approaches including molecular genetics, biology, and biochemistry, I devote my energy to understanding how neurons degenerate in degenerative diseases such as Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS), and frontotemporal lobe degeneration (FTLD). Neurodegenerative diseases preferentially affect one subset of neurons at early stages, but often involve the other neurons at late stages. Comparative study of neurodegenerative diseases may help understand disease mechanisms underlying neurodegeneration and thus help develop effective therapies for these devastating diseases.

The laboratory is currently engaged in three areas of inquiry:

1). Generation of transgenic mouse and rat models for PD and understanding of disease mechanisms underlying dopaminergic neuron death caused by pathogenic mutation in the LRRK2, PINK1, and alpha-synuclein genes

2). Generation of transgenic and knockout rat models for ALS and FTLD and mechanistic study of neurodegeneration in the mutant rats with the TDP-43, the FUS, or the OPTN gene overexpressed or deleted

3). Screening of effective chemicals targeting TDP-43 or FUS for treating ALS

Publications

Most recent Peer-reviewed Publications

1. Reactive astrocytes secrete lcn2 to promote neuron death
2. Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats
3. Mutant TDP-43 in motor neurons promotes the onset and progression of ALS in rats
4. Early exposure to paraquat sensitizes dopaminergic neurons to subsequent silencing of PINK1 gene expression in mice
5. Temporal expression of mutant LRRK2 in adult rats impairs dopamine reuptake
6. TDP-43 potentiates alpha-synuclein toxicity to dopaminergic neurons in transgenic mice
7. FUS transgenic rats develop the phenotypes of amyotrophic lateral sclerosis and frontotemporal lobar degeneration
8. Transgenic rat model of neurodegeneration caused by mutation in the TDP gene
9. Nerve injection of viral vectors efficiently transfers transgenes into motor neurons and delivers RNAi therapy against ALS
10. Developing tTA transgenic rats for inducible and reversible gene expression
11. A tightly regulated Pol III promoter for synthesis of miRNA genes in tandem
12. A construct with fluorescent indicators for conditional expression of miRNA
13. Therapeutic gene silencing delivered by a chemically modified small interfering RNA against mutant SOD1 slows amyotrophic lateral sclerosis progression
14. Allele-specific RNAi selectively silences mutant SOD1 and achieves significant therapeutic benefit in vivo
15. Multiple shRNAs expressed by an inducible pol II promoter can knock down the expression of multiple target genes
16. Transgenic RNAi: Accelerating and expanding reverse genetics in mammals
17. Pol II-expressed shRNA knocks down Sod2 gene expression and causes phenotypes of the gene knockout in mice
18. Pol II-expressed shRNA knocks down Sod2 gene expression and causes phenotypes of the gene knockout in mice.
19. An RNA polymerase II construct synthesizes short-hairpin RNA with a quantitative indicator and mediates highly efficient RNAi
20. Dominant disease gene gets silenced

View All Publications