Now, two groups of scientists have independently found a new component of that braking machinery, adding to understanding of the regulation of neuronal regeneration and of possible treatments to switch off the brakes on regrowth of spinal cord or brain tissue.
The two groups--one group led by Jong Bae Park, Glenn Yiu, and colleagues from Children's Hospital Boston and the other led by Sha Mi and colleagues of Biogen Idec, Inc.--discovered that a protein variously called TAJ or TROY acts as an important part of the receptor on neurons that responds to growth-inhibitory molecules in myelin. Specifically, these molecules prevent the growth of the cablelike axons of injured neurons. Myelin is the fatty sheath that encases neurons and acts as an insulator and aid to the transmission of nerve impulses.
Researchers knew that CNS neurons had receptors on their surface that accepted the inhibitory molecules--like a key fitting a lock--and switched-on inhibitory signaling within the neuron. They had also shown that a protein called p75 could function as a component of the complex of proteins that make up this receptor. The puzzle, however, was that p75 is not widely made in the adult neurons in which this inhibitory receptor complex is known to function.
The two research groups turned their attention to TAJ/TROY because it is a member of the same family of receptor proteins--called TNF receptors--as p75. Their experiments revealed that TAJ/TROY is produced throughout the adult brains of mice. Also, they found that TAJ/TROY readily fits into the inhibitory receptor complex and that the resulting receptor complex switches-on the inhibitory
Contact: Heidi Hardman