Dong Feng Chen, Ph.D., M.D.
Associate Professor of Opthalmology
20 Staniford Street
Boston, MA 2114
Why cannot neurons in the mature retina or central nervous system (CNS) of mammals be regenerated after injury? Is the regenerative failure driven by intrinsic mechanisms of neurons or neural stem cells, or is it a result of changes in the CNS environment? These are not only fundamental issues in basic neurobiology research, but also critical questions in clinical applications.
One part of our work has been dedicated to study the molecular mechanisms that prevent CNS axon regeneration. At a certain point in development, axons in the mammalian CNS lose their ability to regenerate after injury. Using the optic nerve model, we have shown that the absence of intrinsic, Bcl-2-supported mechanisms of axonal growth and the induction of reactive glial cells after injury are two essential elements in adult CNS regenerative failure. Our current efforts aim to combine these paradigms to design therapeutic strategies for treating diseases and damages involving optic nerve or spinal cord damage.
In addition, many neurodegenerative diseases, such as Alzheimer’s disease, Parkingson’s disease, glaucoma, and age-related macular degeneration, share a common tragic feature – neurons die; hence the functions carried out by these neurons are lost. Previously, it is believed that neural stem cells present only in restricted regions in the brain, and the rest of the CNS has very limited ability to regenerate. Recent findings resulted from our research suggest that endogenous neural stem cells are distributed widely throughout the CNS, including the retina, brain and spinal cord, and they can be activated to generate new neurons and enhance CNS function. Currently, my group is devising strategies to activate the dormant capacity of these stem cells in the adult brain and retina. The results of these studies will have important implications for the development of therapies to repair the CNS/retina after trauma, stroke, and other insults and diseases.
For a complete listing of publications click here.