A look at ageing mice has helped researchers dig deep into the biology of itching, revealing differences in skin receptors that help explain not only why some experience irritation, but why it gets worse as we get older.

Medical researchers from Washington University School of Medicine in St Louis have found the pathological sensation known as mechanical itching – or in medical jargon, alloknesis – is associated with a loss of touch receptors in our skin.

"Itching caused by touch becomes more common as we age and is especially problematic for people with dry skin or who already suffer from chronic itching," says anaesthesiologist and senior researcher Hongzhen Hu.

Not only is this annoying for those who experience this problem, but some even risk tearing more delicate skin with overly vigorous scratching.

The kind of itch we get from a mosquito bite is caused by a rush of histamines, chemicals that alert our bodies to an irritation.

Antihistamine drugs can be a solution, but unfortunately these kinds of topical treatments are little help for mechanical itching, leaving sufferers to avoid the touches that are likely to set them off in the first place.

To establish if age really was a factor, the researchers lightly poked a bunch of younger and older mice with a nylon thread, noting it was mostly the aged individuals that responded with a quick scratch.

By comparison, other irritating actions such as jabbing them harder with the same thread, turning up the heat, and even dripping itch-inducing histamines onto their skin elicited the same responses, regardless of how old they were.

Drying the skin on the test subjects' paws with a solution made of acetone and ether also got them scratching, further emphasising links between alloknesis, skin hydration, and ageing.

This all pointed to the involvement of a type of touch receptor called a Merkel cell, which is found in varying densities all over the body just under the skin's surface.

On closer inspection the researchers found these cells indeed decline in numbers in the skins of older mice, and the mice with dry skin.

"As the number of Merkel cells went down, problems with touch-related itch went up," says Hu.

To make sure low numbers of these touch sensors really had something to do with the itch, the team engineered mice without any Merkel cells. And once again, they had some incessant scratchers on their hands.

Stimulating Merkel cells in another group of specially engineered mice alleviated the response, suggesting their activity plays some role in suppressing the itch in most of us.

Getting down to specifics, the team found a protein channel in the membranes of Merkel cells called Piezo 2 was key to their itch-blocking power.

Exactly how all of this fits into a bigger picture on why we itch is still to be figured out, but these are some promising first steps.

Our nervous system has a tough job needing to determine which touches demand an urgent response and which are a distraction we can ignore, and Merkel cells Piezo 2 proteins seem to play a central role in managing this.

"What exactly Merkel cells do has not been clear, but our findings suggest they help control the itch response," says Hu.

"When you lose these cells, their ability to inhibit itch also is lost."

This discovery could one day lead to some form of therapy or pharmaceutical treatment for those who have too few of those special receptors.

Before that can happen, scientists will need to be sure that their mouse models closely match up with human biology.

Hu and his team are planning on doing just this, and are now collecting skin samples from patients diagnosed with alloknesis.

This research was published in Science.

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