A mutated Neanderthal gene could make some people more sensitive to pain


Scattered throughout the genomes of humans around the world, we can find remains of Neanderthal descent. In some, this grants disease resistance, or even a unique head shape. A few have apparently inherited the sensitive side of Neanderthals.

Evolutionary geneticists have closely examined a genetic variation in the DNA of Neanderthals that are known to play a role in generating impulses in some nerves, concluding that this particular form of the gene made them likely to feel more pain.

A search through a database of half a million modern British genomes revealed that about 0.4 percent of people still carry a copy of this mutated version.

Indeed, people who carried the gene also tend to experience more pain symptoms than the average Brit.

It’s the kind of work we’ve only been able to do in the past few years, as improved sequencing technology has revealed unprecedented details of DNA extracted from the remains of Neanderthal.

Among the sequences deciphered by the team was a gene responsible for making a protein called Nav1.7; The work was led by Svante Pääbo at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, along with Hugo Zeberg of the Karolinska Institute in Stockholm.

Located within the membrane of a nerve cell, Nav1.7 functions as a gateway for sodium, ultimately playing a key role in determining the trigger point for impulses that we interpret as painful.

Without this channel, we would feel no discomfort at all. But some variations of Nav1.7 tip sensitivity in the other direction, unlock much more easily and lead to chronic pain.

“People described it as a volume knob, establishing pain gain in the nerve fibers,” Zeberg explained to Ewen Callaway in Nature News.

The researchers discovered that a version of this gene found in the Neanderthal genomes has mutations that would change three amino acids in the protein. To determine if these changes would make a big difference in Nav1.7 function, they inserted the sequence into frog eggs and human kidney tissue.

It was evident that changing any of the amino acids would not be a big problem.

But those three changes together turned Nav1.7 into a happy trigger channel capable of initiating painful impulses much sooner than non-silenced forms.

Despite indications that the Neanderthal form of Nav1.7 is associated with increased pain in modern humans, the results cannot tell us what Neanderthals might have felt, let alone why this sequence evolved in the first place.

Pain is a complex phenomenon that involves a complete set of genes responsible for a variety of processes, with subtle differences that improve sensations in some people and eliminate any form of discomfort in others.

We are pretty sure the Neanderthals felt discomfort, given the evidence of pain relievers found embedded in their plaque. Signs of injury were also common among Neanderthals, along with clear indications of great care in caring for the sick to regain health.

So if we were to take the liberty of speculating a bit, it’s not hard to imagine that turning that pain volume knob up could have been helpful to our robust hominin cousins, faced with trauma in some pretty brutal environments.

Rather than deal with the consequences of antagonizing an injured limb by walking on it or further inflaming an infected tooth, Neanderthals could have rested earlier, perhaps relying on a strong network of family members to help them heal quickly.

Searching for clues in the rest of their genome could tell us more about how they lived their lives.

Given the frequency with which the two branches of our family tree were procreated, understanding their genes also provides us with a clearer understanding of our own history.

It is a pity that Neanderthals disappeared when they did. They could have taught modern humans one or two things about getting along with sensitivity.

This research was published in Current biology.

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