“This gives us a mechanistic explanation for why the transition to chronic pain happens when it does and a real handle on how to intervene,” says Daniele Piomelli, Distinguished Professor of anatomy and neurobiology, who led the study. “The goal isn’t simply to treat pain once it has become chronic; it’s to catch the process while it’s still reversible.” Michael Der
- Researchers discovered that after an injury, support cells are temporarily rewired to trigger nerve cells to produce sticky beta-amyloid protein fragments best known for their role in Alzheimer’s disease.
- In mice, blocking this process shortly after injury prevented pain from becoming persistent without dulling the initial, acute pain response.
- The findings, published in Science Translational Medicine, point to possible targets for future medicines designed to head off chronic pain rather than just mask it.
UC Irvine researchers find that surprising biological pathway plays key role
September 6, 2026 – Irvine, Calif. — Chronic pain is one of medicine’s most stubborn puzzles. A sprained back, a surgical incision or a pinched nerve heals – and yet, for millions of people, the pain never fully goes away. Why some injuries fade into memory while others evolve into a lifelong condition has remained largely a mystery.
A new study from researchers at the University of California, Irvine offers a striking possible answer, and it comes from an unexpected direction: the same amyloid biology long associated with Alzheimer’s disease. The study, which appears in Science Translational Medicine, suggests that chronic pain may be driven by a distinct biological process that begins shortly after injury. If the same pathway is confirmed in people, future treatments might aim to prevent pain from becoming long-lasting rather than only managing it after it’s established…