Scientists have long suspected that genetic factors can predispose certain people to experience chronic pain in intensities others don’t. But now research has backed this up by identifying the specific genetic mark-up scientists think may be responsible.
Researchers at the Children’s Hospital Boston have reported on a novel human pain gene. People with minor variations in this gene showed clear differences in susceptibility to acute heat pain and chronic back pain. The discovery, uncovered in a genome-wide hunt for pain genes in fruit flies, will lead to the development of new pain medication, the identification of risk factors for chronic pain and improved decision-making about the suitability of surgical treatment for different patients, according to Clifford Woolf, director of the F.M. Kirby Center and Program in Neurobiology at the Children’s Hospital Boston.
Nearly 12,000 genes were targeted for mutations specifically in nerve cells, using RNA interference (RNAi) technology.
The team then exposed the different mutant flies to noxious heat, and identified the ones that failed to fly away – and focused on those with mutations that appeared to be specific to pain.
They found that a member of the family of calcium channels should be studied further. Other studies with mice demonstrated that this gene controls sensitivity to noxious heat in mammals as well as flies.
In addition to this, functional MRI imaging revealed that it controls the processing of thermal pain signals in the brain: the heat pain signal seems to arrive appropriately at the thalamus, an early processing centre, but does not travel to higher order pain centers in the cortex.
Together with colleagues at the University of Pittsburgh and the University of North Carolina, the team looked at four single nucleotide polymorphisms (SNPs), and found that certain less common SNPs were associated with reduced sensitivity to acute pain in a test administering a quick series of noxious heat pulses.
The international team plans further studies on the other pain genes identified in the fly screen.
In 2006, Clifford Woolf’s team identified the first pain sensitivity gene in humans, GCH1. “We are trying now to use a panel of the pain genes we’ve found— alpha 2 delta 3, KCNS1, GCH1 and others—to develop a genetic risk profile and then say, if you combine these polymorphisms you have a 60% chance of chronic pain after surgery, versus say, if you have another polymorphism mix, a 5% chance. This is another way to personalise medicine,” Woolf says.
Woolf has spoken about the role of genetic research in treating chronic pain: “Across a number of different kinds of pain, genes seem to be at least half the driver of how much pain you experience. Genes give us an amazing and powerful tool to begin to understand how pain is generated, and which functional pathways and specific proteins are involved,” he said.
While this is a significant development, it does not mean that scientists are about to develop effective ways to use genetic therapy to quell chronic pain. But it’s the latest finding in a long line of research and observation of the so-called pain gene that goes back almost a decade and will help us to better understand how and why pain occurs.
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