Researchers at the University of California, Irvine (UCI) have identified a surprising biological pathway that may help explain how temporary pain develops into chronic pain.
The study, published in Science Translational Medicine, found that after an injury, changes in cells called oligodendrocytes in the spinal cord can contribute to nerve damage and trigger the production of a protein called beta-amyloid 42 (Aβ42). This is notable because beta-amyloid is better known for its connection to Alzheimer’s disease.
Researchers conducted the experiments in mice and observed that beta-amyloid levels increased during the period when short-term pain was transitioning into persistent pain. When scientists blocked the production or activity of beta-amyloid through several different approaches, the mice did not develop chronic pain, while their initial response to injury remained intact.
The team also identified an enzyme called N-acylethanolamine acid amidase (NAAA) as an important part of the process. When the researchers removed this enzyme specifically from oligodendrocytes, the animals were protected from the increase in beta-amyloid and subsequently did not develop chronic pain in the experimental models.
The findings could eventually lead to a different approach to pain treatment—preventing chronic pain during the early period after an injury, rather than treating it after it has already become established.
However, researchers stressed that the findings have so far been demonstrated in animal models, and it remains necessary to determine whether the same pathway occurs in humans and whether it can be safely targeted. The researchers also cautioned that existing Alzheimer’s or amyloid-targeting medicines should not be used off-label for pain based on these findings alone.
The study provides a potential new direction for chronic pain research and raises the possibility that the transition from acute to chronic pain may be biologically preventable if the process can be identified and interrupted early enough.
