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 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 in male and female mice.

“Delineating the nature, localization and timing of the events involved in pain chronicity is necessary to pinpointing control nodes in the process that can be targeted by new classes of disease-modifying medicines beyond analgesics,” said Daniele Piomelli, Distinguished Professor in the UCI School of Medicine Department of Anatomy & Neurobiology. “This study is the first to identify that NAAA, a previously unrecognized control node, can be effectively targeted by small-molecule therapeutics that inhibit this enzyme, and block the transition from acute to chronic pain.”