Blocking Pain Progression

In an effort to uncover therapies that will modify diseases, researchers sought a better understanding of precipitating molecular events. Reporting their findings in the journal of Science Advances, the scientists found that immobilizing N-acylethanolamine acid amidase (NAAA) at a specific time restores normal palmitoylethanolamide (PEA), an endogenous lipid agonist of the nuclear receptor peroxisome proliferator–activated receptor-α (PPAR-α), which “stops metabolic reprogramming, and aborts the transition to pain chronicity. This action identifies NAAA and its cognate signaling complex as a druggable molecular target for the prevention of chronic pain.”

Daniele Piomelli, Distinguished Professor in the UCI School of Medicine Department of Anatomy & Neurobiology, and coauthor of the study, commented: “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. 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.”

 

Read the journal article.

Read the press release.

Other Categories:

• chronic pain

• clinical trials

• research/study

• spinal/spine