Source : INDIA TODAY NEWS
Chronic nerve pain can be difficult to treat. Unlike pain caused by a temporary injury, neuropathic pain can continue for months or even years after the original nerve damage has occurred. For many people, commonly used pain medicines provide limited relief, while some treatments can cause side effects that affect everyday life.
Now, researchers have identified a possible new pathway involved in chronic nerve pain. A study from researchers at The University of Texas MD Anderson Cancer Centre has found that a protein called BRAF, which is already well known for its role in cancer, may also play an important part in increasing pain signals after nerve injury.
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The findings are particularly interesting because medicines that block BRAF are already used in cancer treatment. In experiments involving preclinical models, blocking BRAF signalling reduced sensitivity to pain. This raises the possibility that existing cancer drugs could eventually be studied for treating certain forms of chronic nerve pain.
However, experts caution that this is still early research. The findings have not yet established BRAF inhibitors as a treatment for people with chronic pain, and clinical studies in humans will be needed to determine whether the approach is safe and effective.
BRAF MAY HELP TURN NERVE DAMAGE INTO PERSISTENT PAIN
Neuropathic pain can develop when nerves are damaged because of an injury, disease or certain medical treatments. Cancer patients, for example, can experience nerve pain as a side effect of some chemotherapy medicines.
Researchers wanted to understand why pain can become stronger and persist long after the initial nerve damage.
Their study focused on NMDA receptors, which are protein channels involved in communication between nerve cells in the brain and spinal cord. Following nerve damage, these receptors can become excessively active and amplify pain signals travelling towards the brain.
The researchers found that BRAF appears to be involved in this process.
After nerve injury, BRAF was found to travel through sensory nerve cells towards their endings in the spinal cord. There, it helped activate signalling that increased the activity of NMDA receptors.
This could make the nervous system more sensitive to pain and contribute to the development of chronic neuropathic pain.
The researchers also found evidence of a relationship between BRAF-related proteins and NMDA receptors in human spinal cord tissue.
BLOCKING BRAF REDUCED PAIN SENSITIVITY IN PRECLINICAL MODELS
The researchers then looked at what happened when BRAF signalling was blocked.
In preclinical models of nerve injury, inhibiting BRAF reduced pain sensitivity. This suggests that BRAF may not simply be associated with nerve pain but could actually be involved in the biological process that strengthens pain signalling.
The researchers say their findings identify BRAF as a potential target for future neuropathic pain treatments.
The study was co-led by Shao Rui Chen, M.D., professor of Anaesthesiology and Perioperative Medicine, and Hui Lin Pan, M.D., PhD, endowed chair of Anaesthesiology and Perioperative Medicine. The research was published in Science Signaling.
WHY CANCER DRUGS ARE BEING CONSIDERED FOR PAIN
One of the most interesting aspects of the research is that BRAF is already a well-established target in cancer treatment.
BRAF inhibitors have been developed and approved for certain cancers. Because medicines targeting this protein already exist, researchers may have a potential starting point for investigating whether the same pathway can be targeted to control chronic nerve pain.
The idea is not that cancer patients should start taking these medicines for pain. Instead, the discovery gives researchers a possible pathway to investigate further.
If future studies confirm that BRAF inhibitors can safely reduce abnormal pain signalling in humans, these medicines could potentially be repurposed or could help guide the development of new treatments specifically designed for neuropathic pain.
CANCER TREATMENT CAN ALSO CAUSE NERVE PAIN
The findings may be particularly relevant to cancer patients because some cancer treatments can themselves cause nerve damage.
Chemotherapy-induced peripheral neuropathy can lead to symptoms such as burning pain, tingling, numbness, sensitivity to touch and shooting or electric shock-like sensations. These symptoms can sometimes continue even after cancer treatment has ended.
Researchers at MD Anderson have previously investigated how chemotherapy-induced nerve pain is linked to changes in NMDA receptor activity.
The new findings add BRAF to this picture and suggest that the protein may be part of the pathway through which nerve damage eventually produces stronger and persistent pain signals.
THE FINDINGS ARE PROMISING BUT STILL EARLY
Despite the potential, it is important not to interpret the study as proof that cancer drugs can currently treat chronic nerve pain.
The research was conducted primarily in preclinical models. Results seen in laboratory and animal studies do not always translate into the same benefits in people.
BRAF inhibitors also have their own potential side effects and are prescribed for specific cancer indications. Their safety, dosage and long-term effects would need to be carefully evaluated if they were to be considered for chronic pain.
The next major step will therefore be clinical research involving people with neuropathic pain.
If human studies eventually show that blocking BRAF can safely reduce persistent pain, the discovery could open up an entirely new treatment strategy. Instead of only trying to reduce the sensation of pain, future therapies could potentially target one of the biological pathways responsible for amplifying pain signals in the first place.
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SOURCE :- TIMES OF INDIA
