Jianhua Zhang, Ph.D.


Associate Professor


Primary Department Affiliation
: Pathology
Primary Research Area: Neurodegeneration and Neurodegenerative Disorders

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Phone: 205.996.5153
Fax: 205.934.7447

Recent Publications


Dr. Zhang graduated from University of Science and Technology of China. She received her PhD from University of Texas Southwestern Medical Center at Dallas in 1991. She then worked as a postdoctoral associate in the Whitehead Institute for Biomedical Research from 1991 to 1995. Before joining UAB, she worked as a Research Assistant Professor in University of Cincinnati College of Medicine from 1996 to 2005.

Excessive stimulation of glutamate receptors induces neuronal cell death during development, as well as in patients with epilepsy, traumatic brain injury, ischemia, hypoglycemia, and various neurodegenerative diseases. How activation of glutamate receptors and subsequent calcium influx initiate intracellular signaling, alter gene expression, and turn on cell death machineries in response to developmental and environmental cues is unclear. We are using both in vivo and in vitro models to identify signaling pathways that mediate or protect against excitotoxicity to eventually help design better strategies for prevention and treatment of neurological and psychiatric diseases.

Parkinson's disease (PD) is the most common age-related movement disorder and the second most common neurodegenerative disease. PD currently affects more than 500,000 people in the US, and the total financial cost to the nation is estimated to exceed $6 billion per year. Five to 10 percent of PD is early-onset and often inherited, some of these resulting from known genetic mutations in alpha-synuclein, Parkin, DJ-1, PINK1, or DRDN. PD neuropathology includes two main features: a) accumulation of Lewy bodies that consist largely of ubiquitin and alpha-synuclein aggregates in affected neurons, and b) progressive loss of nigrostriatal dopaminergic neurons. The objective of our research is to identify environmental and genetic triggers for Lewy body formation and dopaminergic neuron death, and ultimately identify strategies for prevention and treatment of PD.