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Comment
. 2013 Mar;154(3):326-327.
doi: 10.1016/j.pain.2012.12.012. Epub 2012 Dec 28.

N-acylethanolamine acid amidase (NAAA), a new path to unleash PPAR-mediated analgesia

Affiliations
Comment

N-acylethanolamine acid amidase (NAAA), a new path to unleash PPAR-mediated analgesia

Bradley K Taylor. Pain. 2013 Mar.
No abstract available

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Conflict of interest statement

The author has no conflicts of interest

Figures

Figure 1
Figure 1
Proposed mechanism of pain inhibition by N-acylethanolamine acid amidase (NAAA). Panel A: key enzymatic pathways for fatty acid ethanolamide synthesis and degradation (solid black arrows), and a proposed mechanism of pain inhibition involving palmitoylethanolamide (PEA) activation of PPARα (blue arrows), and PPARα-mediated pain inhibition (green arrows). Panel B: Injury-induced inhibition of the enzyme that synthesizes PEA (N-acyl-phosphatidylethanolamine phospholipase D, NAPE-PLD) and ensuing loss of PEA-PPARα antihyperalgesia. Panel C: Inhibition of N-acylethanolamine acid amidase (NAAA) with the novel compound ARN077 raises PEA concentrations, thus reinstating PPARα antihyperalgesia. PE, phosphatidylethanolamine. PC, phosphatidylcholine. NAT, N-acetyltransferase. NAPE, N-acylphosphatidylethanolamines. AEA, arachidonoylethanolamide (anandamide). OEA, oleoylethanolamide. AA, arachidonic acid. OA, oleic acid. PA, palmitic acid. EA, ethanolamine.

Comment on

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