Previously unrecognized control point identified as target for drugs that block transition.
A new study led by University of California, Irvine researchers is the first to reveal the specific molecular mechanism that controls the transition from acute to chronic pain, and identifies this mechanism as a critical target for disease-modifying medicines.
Findings from the study, titled “NAAA-regulated lipid signaling governs the transition from acute to chronic pain,” published today (October 22, 2021) in Science Advances, show that disabling N-acylethanolamine acid amidase (NAAA)—an intracellular enzyme–in the spinal cord during a 72-hour time window following peripheral tissue injury halts chronic pain development …
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