Han, who is majoring in neuroscience, was among 42 Johns Hopkins students to receive a Provost's Undergraduate Research Award to finance his research in the 2001-2002 academic year. He presented results from his research at a campus awards ceremony March 7.
Researchers had thought for many years that mature nerve cells either wholly or partially located in the brain or the spinal cord could not regenerate after damage to their branches, which are known scientifically as axons. They had identified a family of proteins known as myelin-associated proteins, prevalent in the brain and spine, and shown in the laboratory that these proteins blocked growth of new axons in mature nerve cells.
However, those same inhibitory compounds cannot block the growth of new axons on immature nerve cells. And scientists have found a couple of circumstances that seem to push mature nerve cells towards states where their regenerative ability returns.
For example, Han’s mentor Paul Hoffman, an associate professor of ophthalmology, showed that a slightly altered version of a naturally occurring compound could restore regenerative ability in the laboratory to axons of mature nerve cells that entered the central nervous system. That altered form of the naturally occurring compound is known as db cAMP.
While many researchers in the field emphasize the inhibitors in the central nervous system and other environmental factors as the main roadblocks to regeneration, Hoffman and Han suspect intrinsic differences between mature and immature nerve cells may be key contributors. Han used his Provost’s Award to further probe how closely mature neurons that had been newly enabled to regenerate axons in the central nervous system resembled the immature neurons that could always do so.
He did this by testing rates of axon regeneration in the sciatic nerves of rats. Other scientists had shown that regeneration rates of axons outside the central nervous system could be increased by physically squashing another axon of the same nerve cell, a stimulus known as a conditioning lesion.
Were conditioning lesions activating the same regeneration mechanisms that the db cAMP used earlier by Hoffman’s lab had activated? Han found they weren’t; in a direct comparison, db cAMP couldn’t cause injured sciatic nerve axons to grow back as quickly as conditioning lesions could.
Although there are still many more unanswered questions about nerve cell regeneration in the central nervous system than answered questions, Hoffman said Han's results are an important step forward for researchers who hope to one day be able to develop new clinical treatments for optic disorders involving nerve degeneration or injury, or for spinal cord injuries.
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