Jefferson Alumni Hall, Suite 508
Philadelphia, PA 19107
(215) 503-1037
Most Recent Peer-reviewed Publications
- Entorhinal cortical neurons are the primary targets of FUS mislocalization and ubiquitin aggregation in FUS transgenic rats
- Mutant TDP-43 in motor neurons promotes the onset and progression of ALS in rats
- Early exposure to paraquat sensitizes dopaminergic neurons to subsequent silencing of PINK1 gene expression in mice
- Temporal expression of mutant LRRK2 in adult rats impairs dopamine reuptake
- TDP-43 potentiates alpha-synuclein toxicity to dopaminergic neurons in transgenic mice
Medical School
MD (equivalent), Hunan Medical University, China - 1990
MS, rehabilitation and physical therapy, Hunan Medical University, China
- 1995
PhD (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:
- 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
- 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
- Screening of effective chemicals targeting TDP-43 or FUS for treating ALS
