“With physical disability also comes psychological disability. Perhaps if we can mend the body, we can heal the soul.”

This article provides critical insights into how regeneration is inhibited in the adult central nervous system by myelin components. We demonstrated that a novel molecule, LINGO-1, is required to form a functional signaling complex with Nogo-66 receptor and p75, to transduce the myelin inhibitory signal. Until this report, there was a missing component of this signaling complex and its function could not be reconstituted. We now have a molecular basis for understanding how axonal regeneration is inhibited. Elucidation of this pathway opens the doors for the treatment of diseases involved in nerve degeneration, such as spinal cord injury or brain trauma.

This article presents a new discovery of an important component of the Nogo-66 receptor complex, which leads to a better understanding of myelin inhibitory signals that prevent axonal growth and regeneration.

The central nervous system (CNS) cannot grow back after injury, and so paralysis and loss of sensory functions can result. Why the CNS cannot grow back has been a critical research focus amongst neurobiologists for nearly a century. We found that a protein called LINGO-1 helps explain the inability of CNS to regenerate. By identifying drugs that can block LINGO-1, we hope to encourage damaged neurons to grow as a way of treating CNS diseases or injury.

This work started as part of a drug discovery effort at Biogen Idec, a company with a very strong interest in neurological diseases such as multiple sclerosis. Our team is involved in identifying the functions of new molecules related to human neurological diseases.

There is a vast economic cost to CNS disease or trauma that is associated with hospitalization, rehabilitation, long-term nursing care and psychological disability.