For decades, researchers have been trying to discover the root of pain, and thanksto a newstudypublished this week, scientists have come one significant step closer: They have identified a single gene that may be at the root of many cases of a condition called congenital insensitivity to pain (CIP).
From the time they’re born, people with CIP don’t feel any pain at all.
The newly-discovered gene, called PRDM12, isn’t the first that’s been found to be linked with pain. What makes this gene special is the fact people with the mutation experience few — if any — other side effects. That makes it, in the words of Cambridge University genetics professor and lead study author Geoff Woods, a “super-duper pain target.”
In other words, it could be the perfect candidate for a new kind of painkiller.
Knowing how this tweak works could help scientists create a more efficient, longer-lasting class of pain medications with potentially minimal side effects.
The problem with living without pain
A life without pain sounds ideal at first. No migraines, no achy joints, no searing agony when an over-filled cup of hot coffee burns your hand.
But it’s not as great as it sounds.
Because they don’t recoil at the touch of a hot stove or stop walking on an injured foot, for example, people with a mutation to the PRDM12 gene can — and often do — get injured pretty badly.
Out of the 158 people from 11 families across the globe with the mutation that the researchers looked at for their study, many suffered from mutilated lips and tongues, wounded or partially-missing fingers and toes, and blistered or scarred skin.
These people had two mutated copies of the PRDM12 gene (we get one copy of each of our genes from our mums and another copy from our dads, and people with just one defective copy were unaffected). Not only have they never felt any kind of physical pain, but they also can’t tell the difference between extremely hot and cold temperatures.
No nerve endings, no pain
When the researchers took a deeper look at these peoples’ skin, they found something striking: They were all missing nerve endings, the bundles of fibres responsible for sending information about the outside world to our brains and a pretty vital component of pain sensation.
They also found that in one of the sensory nerves in their legs, they only had about half the normal number of the special fibres that alert us to pain.
Since the mutation appeared to effect the development of specific parts of the body we need to feel pain, the scientists also took a look at how the gene developed in the womb using frog and mouse embryos. The PRDM12 gene, they confirmed, appears to play a vital role in helping us develop the cells that tell us when something hurts.
This isn’t the first gene that scientists have found is linked with the inability to feel pain from birth.
Tweaks in two other genes also appear to cause the condition, but these shifts work by preventing pain fibres from sending pain signals to the brain, rather than by blocking the growth of the fibres that detect pain in the first place.
The researchers think PRDM12 could be the key to helping millions of pain sufferers around the world.
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