Zhigang He

Zhigang He

Professor of Neurology
Zhigang He

Restoring lost function after spinal cord injury or other types of CNS injuries is a major challenge of contemporary neuroscience. A key culprit of functional deficits is the disruption and/or dysfunction of axonal connections connecting different parts of CNS. In order to develop novel neural repair strategies, our research has been addressing the following questions:

First, why axon regeneration fails in the adult mammalian CNS? Our past studies identified key molecular players, such as PTEN and SOCS3, in controlling the intrinsic regenerative ability of neurons. Currently, we are interested in understanding how these and other molecular pathways regulate axon regeneration in cellular and molecular terms. Furthermore, our current studies, by using models of optic nerve injury and spinal cord injury, aim to maximize the extent of neuronal survival and axon regeneration and enhance their functional integration.
Second, anatomical axon regeneration does not automatically translate into functional recovery. For example, most regenerated axons in injured optic nerves are not myelinated, representing a major hurdle for axonal conduction and functional restoration. In addition, although anatomically spared axons are present in many spinal cord injury patients, they are often functionally silent and fail to show compensatory function. We are actively exploring cellular and molecular mechanisms that promote re-myelination and enhance functionality of regenerated and/or spared axons.
Third, in order to design tailored neural repair strategies after spinal cord injury, another direction in the lab is to crack the code of the control of the spinal cord function by the brain, by dissecting the physiological function of different spinal descending projections. While our recent efforts dissected the role of cortex-derived corticospinal axons in skilled motor control and sensory processing, we are continuing to study the function of brainstem-derived reticulospinal and other descending projections. Characterizing how these descending inputs control motor output and integrate sensory in determining the functional outputs of the spinal cord will help design rational strategies of promoting functional recovery after injury.
Together, we expect that answering these questions will establish important principles for exploiting regenerative medicine to treat CNS injury and other neurological diseases.


Contact Information

Boston Children's Hospital
F.M. Kirby Neurobiology Center
Center for Life Science, Room 13-076
3 Blackfan Circle
Boston, MA 02115
p: 617-919-2353