It's known that the development of neuronal diseases such as multiple sclerosis and Alzheimer's disease is connected with the levels of myelin - an insulating substance around nerve fibres - in the body, although the actual causes of these conditions remain unknown. Now researchers at IBEC have discovered a new group of interacting partners for myelin-associated receptors, which could shed light on the significance of imbalanced production or modifications of the substance.
In a study published online by the FASEB journal this week, group leader José Antonio del Río, together with his postdocs Vanessa Gil and Franc Llorens, have been looking at axons, ligands and receptors in the mammalian central nervous system. Following injury in adults, axons have a limited capacity for regrowth; this restriction is caused by myelin-associated inhibitors (MAIs).
A release from myelin inhibition thus improves neuronal regeneration, and the three researchers from IBEC's Molecular and Cellular Neurobiotechnology group have discovered that blocking two of some of these proteins' shared receptors - NgR1, together with its coreceptors p75(NTR), TROY and Lingo-1, and paired immunoglobulin-like receptor B (PirB) - prevents the inhibitors from restricting axonal sprouting and limiting the regeneration of damaged fibre tracts.
Other elements of the myelin inhibitory pathway are still unknown, but this identification and characterization of the roles and functions of some of the inhibitory molecules sheds light on one of the most competitive areas of research into neuroregeneration of the past several years. In addition, further data from within and outside the CNS environment suggests that most of these proteins have other roles beyond axonal growth inhibition.
"Potentially there could be new physiological roles for them in other processes such as development, neuronal homeostasis, plasticity and neurodegeneration," says José Antonio. "Modifications could be considered as markers for certain neuronal diseases."
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