Zhigang He
From Wikipedia, the free encyclopedia
- Ameritec Prize (2005)
- Reeve-Irvine Research Medal (2019)
- Greenberg END Blindness Initiative, Visionary Award (2020)
- National Academy of Medicine (2021)
Zhigang He | |
|---|---|
| Born | c. 1975 (age c. 50) |
| Alma mater | University of Toronto (PhD) |
| Known for | Axon regeneration, spinal cord injury research |
| Awards |
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| Scientific career | |
| Fields | Neuroscience, Neurology, Ophthalmology |
| Institutions | Harvard Medical School Boston Children's Hospital |
Zhigang He (born c. 1975) is a Chinese-American neuroscientist and a professor of neurology and ophthalmology at Harvard Medical School. He is known for his research on axon regeneration and the restoration of function following spinal cord injuries and visual pathway injuries. Additionally, his research aims to understand the organizing principles that govern the connections between the brain and spinal cord.[1][2][3]
He received his PhD in Genetics from the University of Toronto in 1996. He then held postdoctoral positions at the University of California, San Francisco. In 2000, he joined the Kirby Center in Neuroscience at Boston Children’s Hospital.[4] He is currently a professor of Neurology and Ophthalmology at Harvard Medical School.[5][6]
Research
His research focuses on regeneration in the central nervous system (CNS), particularly in the optic nerve and spinal cord, as well as the molecular pathways involved in neural repair.[7][8]
He discovered that the PTEN/mTOR and SOCS3/STAT3 signaling pathways are key regulators of the intrinsic growth capabilities of adult neurons.[9] This work led to the development of the first set of manipulations that enable robust axon regrowth in multiple CNS injury models.[10][11]
He investigated the fact that, in many spinal cord injury patients, not all axons are severed; however, the remaining connections often become functionally silent. He found that this functional dormancy is due to injury-induced dysfunctions of the chloride transporter KCC2 in spinal inhibitory neurons.[12][13] Restoring KCC2 activity presents a highly translatable method for reviving the functionality of spared neuronal circuitry in patients with incomplete spinal cord injuries.[14][15]
He optimized methods for systematically labeling spinal-projecting neurons (SPNs) and identified key functional organizations within brain-spinal cord connections.[16] For example, he distinguished specific SPN populations that separately control motor, sensory, or sympathetic functions, as well as those that simultaneously regulate both motor and sympathetic pathways.[17]
