Chronic pain affects more than 50 million people in the United States, and many of them—especially women—live with daily discomfort that current medications cannot relieve.
For years, treatment options have remained limited, particularly for pain that doesn’t come from visible injury or inflammation.
Now, scientists at Virginia Tech have made a breakthrough that could change the lives of millions: they’ve found a way to switch off this kind of pain in female mice by blocking a specific pathway.
In a study published in the journal Pain, neuroscientist Ann Gregus and her team showed that they could erase well-established pain behaviors by targeting an enzyme system in the body.
This system produces molecules that intensify pain. By shutting it down, they were able to restore function and reduce pain, offering a potential new path to non-opioid treatments for chronic pain.
What makes this discovery especially important is that it didn’t just stop pain from developing—it reversed pain that was already present, more closely mimicking the real-life experience of patients who suffer for years.
The type of pain studied is known as nociplastic pain. Unlike pain caused by injuries or inflammation, nociplastic pain comes from changes in how the nervous system handles signals.
Conditions like fibromyalgia, chronic back pain, and some migraines fall into this category. They are very hard to treat, and current drugs often don’t help. Many patients are left frustrated, with limited options other than opioids, which carry the risk of addiction.
Gregus and her team focused on a different target than traditional pain medications. While common drugs like NSAIDs reduce inflammation, they don’t work for nociplastic pain. This new approach targets a separate biological pathway, offering a fresh angle for pain relief.
The discovery came in part by accident. During the COVID-19 pandemic, lab supplies were limited, and the team had to switch to a different strain of female mice. These mice happened to develop stronger and longer-lasting pain responses, giving researchers a better model for studying chronic pain. It was a lucky break that led to a major insight.
Using an immune challenge to simulate chronic pain, the researchers waited until the mice showed clear signs of pain. Then, they gave them compounds developed by the NIH that block specific parts of the enzyme system.
The results were powerful: pain sensitivity disappeared, and muscle strength returned. Giving the pain-triggering molecules alone recreated the pain state, proving their role.
One of the compounds is already being tested in humans for another disease, meaning it could be fast-tracked for use in chronic pain if trials go well.
Gregus, who has suffered from migraines and nerve pain herself, says the motivation is deeply personal. “I know what it’s like to live with pain every day and be told there’s nothing else that can be done,” she shared.
Her lab is now testing whether the same treatment could work for pain caused by chemotherapy or diabetes—conditions that affect millions and often lead to lifelong discomfort. If it works in those cases too, it could be a game-changer.
The dream is to develop a therapy that doesn’t just cover up the pain, but actually reverses what causes it. For patients who’ve heard “there’s nothing more we can do,” this new discovery could one day offer real and lasting relief.
If you care about pain, please read studies about how to manage gout with a low-purine diet, and a guide to eating right for arthritis.
For more health information, please see recent studies about the link between processed foods and chronic diseases, and avoid these 8 foods to ease arthritis pain.
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