PHILADELPHIA - A new animal model of nerve injury has brought to light a critical role of an enzyme called Nmnat in nerve fiber maintenance and neuroprotection. Understanding biological pathways involved in maintaining healthy nerves and clearing away damaged ones may offer scientists targets for drugs to mitigate neurodegenerative diseases such as Huntington's and Parkinson's, as well as aid in situations of acute nerve damage, such as spinal cord injury.
University of Pennsylvanian biologists developed the model in the adult fruit fly, Drosophila melanogaster.
"We are using the basic power of the fly to learn about how neurons are damaged in acute injury situations," said Nancy Bonini, senior author of the research and a professor in the Department of Biology at Penn. "Our work indicates that Nmnat may be key."
The research was published in Current Biology. First author on the study is postdoctoral researcher Yanshan Fang, with additional contributions from postdoctoral researcher Lorena Soares and research technicians Xiuyin Teng and Melissa Geary, all of Penn's Department of Biology.
When a nerve suffers an acute injury -- as might be caused by a penetrating wound, for example, or a broken bone that damages nearby tissues -- the long projection of the nerve cell, called the axon, can become injured and degenerate. The process by which it disintegrates is known as Wallerian or Wallerian-like degeneration and is an active, orderly process.
Though this function of eliminating damaged nerve cells is crucial, biologists do not have a clear understanding of all of the molecular signaling pathways that govern the process.
Bonini's lab has previously focused on chronic neurodegenerative diseases but made this foray into acute nerve injury to determine if mechanistic overlaps exist between acute axon injury and chronic neurodegeneration. They first searched for an appropriate nerve tract to t
|Contact: Katherine Unger Baillie|
University of Pennsylvania