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Study: Nervous System Plays Key Role in Arthritis
Reducing levels of nerve-growth factor may lead to better pain treatments (June 13)
A new study in the Journal of Neuroscience adds to a growing body of evidence that the nervous system and nerve-growth factor (NGF) play a major role in arthritis. The findings also support the idea that reducing elevated levels of NGF — a protein that promotes the growth and survival of nerves, but also causes pain — may be an important strategy for developing treatments for arthritis pain.
Scientists at McGill University in Montreal, Canada, examined inflammatory arthritis in the ankle joints of rats. In particular, they investigated changes in the nerves and tissues around the arthritic joints using specific markers that allowed nerve fibers to be visualized with a fluorescence microscope.
Normally, sympathetic nerve fibers regulate blood flow in blood vessels. Following the onset of arthritis in the rats, however, these fibers began to sprout into the inflamed skin over the joint and to wrap around the pain-sensing nerve fibers instead. Sympathetic fibers were also detected in the arthritic joint tissues.
The results also showed a higher level of NGF in the inflamed skin — mirroring the findings of human studies that have shown increased NGF levels in arthritis patients.
To investigate the role of these abnormal sympathetic fibers, the researchers used an agent to block the fibers’ function. They found that this reduced pain-related behavior in the animals.
“Our findings reinforce the idea that there is a neuropathic component to arthritis, and that sympathetic nerve fibers play a role in increasing the pain,” said Geraldine Longo, a doctoral student, who co-authored the paper with Prof. Alfredo Ribeiro-da-Silva.
Ribeiro-da-Silva added: “We are currently using drugs to prevent the production of elevated levels of NGF in arthritic rats. We hope that our research will serve as a basis for the development of a new treatment for arthritis in the clinic.”
Source: McGill University; June 13, 2013.