Scientists discover how to reverse pain caused by diabetes-related nerve damage

Scientists discover how to reverse pain caused by diabetes-related nerve damage


An international research team has discovered how to reverse the pain caused due to peripheral nerve damage in diabetes. The scientists have identified and successfully tested a molecule that can inhibit the function of a protein that turns touch receptors into pain receptors under the skin. The research in mice paves the way for future research in humans, with scientists hopeful that a new drug can be developed to treat patients with the debilitating condition, diabetic neuropathy, as well as other nerve damage-related pain.

The Senior co-author of the research study said nerve damage generally cannot be repaired, therefore proper pain management  can significantly improve the lives of people with diabetic neuropathy and others living with nerve damage.

The human skin is equipped with specialised receptors that allow the perception of the slightest brush, meaning some of these receptors can even detect extremely small movements. These movements are transformed into electrical signals via channels at sensory endings in the skin. The sensitivity of these channels is controlled by a protein called Stomatin- Like  protein- 3  (STOML3), which is required for normal receptor function.

In  an earlier study, the team identified this protein as a target for blocking pain receptors found underneath the skin. In the latest study, researchers identified a single molecule after searching through a library catalogue of 35,000 compounds.

When this molecule was tested on the sensory endings in the skin of mice, they found STOML3 clustering was inhibited and pain receptors were silenced. Importantly, the scientists found that inhibiting STOML3 did not significantly affect the non-pain-related touch sensitivity of the mice, ensuring touch sensitivity was not sacrificed at the expense of turning off pain receptors.

"While a potential new treatment for the pain associated with diabetic neuropathy is still some years away, the research is an important first step in changing the accepted thinking around how to treat the condition," the senior- co author said. "Directly targeting nerve receptors in the skin could help manage pain in a way that does not trigger the negative side effects of drugs that act on the body's central nervous system, which is how most current treatments work."  Another senior co- author of the study commented that the research represents a new approach arising from an understanding of the mechanisms that turn sensations of touch into pain.

"If human patients respond the same way, this will represent a major step in treating a neuropathology that has a devastating effect on the lives of many people,"  "We will be studying force sensing molecules in the cells that make our cartilage to see if we can identify a way to reverse the cartilage damage that occurs when people develop osteoarthritis, said the co- author. "This also involves going back to the drawing board to look more closely at force sensing proteins in other cells and tissues so we can increase our understanding of how human cells sense their physical surroundings."


http://www.nature.com/neuro/journal/vaop/ncurrent/full/nn.4454.html
 
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