Nearly 1 in 5 people suffers from chronic pain. Understanding why certain people develop pain while others do not is a major challenge. Achieving individualized therapies effective for specific patient populations is yet another challenge.
However, research published online in Nature Medicine may include solutions to both challenges. A major gene affecting chronic pain sensitivity has been identified by a research team led by Prof. Jeffrey Mogil of McGill University in Montreal and Prof. Michael Salter of The Hospital for Sick Children (SickKids), affiliated with the University of Toronto. The discovery may also lead to the individualization of chronic pain treatment.
Researchers identified the gene that encodes the pain receptor P2X7. More specifically, the scientists revealed that a single amino-acid change in P2X7 influences sensitivity to the 2 main causes of chronic pain: inflammation and nerve damage.
The amino-acid change is known to affect only the forming of pores that permit large molecules to pass through P2X7 receptors. Yet, much tinier ions are still allowed to flow through. The researchers found that pain behaviors dramatically decreased, when using a peptide that targets pore formation only.
The scientists then examined genetic differences among human patients suffering from 2 distinct types of persistent pain: chronic post-mastectomy pain and osteoarthritis. In both instances, researchers discovered that individuals with genetically inherited low pore formation in P2X7 receptors experienced lower pain levels.
“Our findings indicate that it may be possible to develop drugs that block pores in this crucial receptor, while leaving its other function intact – thereby killing pain while minimizing side effects,” said Professor Mogil, E.P. Taylor Professor of Pain Research in McGill’s Department of Psychology.
Source: McGill.