Classical and Unexpected Effects of Ultra-Micronized PEA in Neuromuscular Function

Biomolecules. 2022 May 29;12(6):758. doi: 10.3390/biom12060758.

Abstract

Recently, the endocannabinoid system has attracted growing attention from the scientific community for its involvement in homeostatic and pathological processes as they pertains to human physiology. Among the constituents of the endocannabinoid system, the molecule palmitoyl ethanolamide has particularly been studied for its ability to reduce several inflammatory processes involving the central nervous system. Here, we reviewed published literature and summarized the main targets of the palmitoyl ethanolamide, along with its unique possible mechanisms for restoring correct functioning of the central nervous system. Moreover, we have highlighted a less-known characteristic of palmitoyl ethanolamide, namely its ability to modulate the function of the neuromuscular junction by binding to acetylcholine receptors in different experimental conditions. Indeed, there are several studies that have highlighted how ultra-micronized palmitoyl ethanolamide is an interesting nutraceutical support for the treatment of pathological neuromuscular conditions, specifically when the normal activity of the acetylcholine receptor is altered. Although further multicentric clinical trials are needed to confirm the efficacy of ultra-micronized palmitoyl ethanolamide in improving symptoms of neuromuscular diseases, all the literature reviewed here strongly supports the ability of this endocannabinoid-like molecule to modulate the acetylcholine receptors thus resulting as a valid support for the treatment of human neuromuscular diseases.

Keywords: neuromuscular junction; neurophysiology; palmitoyl ethanolamide.

Publication types

  • Review
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Endocannabinoids* / metabolism
  • Humans
  • Neuromuscular Diseases* / drug therapy
  • Receptors, Cholinergic*

Substances

  • Endocannabinoids
  • Receptors, Cholinergic

Grants and funding

This work was supported by the Fondazione Italiana di Ricerca per la Sclerosi Laterale Amiotrofica (AriSLA Grant “MUSALS-AChR”) to E.P. and M.I. This research was supported by intramural “DISCAB” GRANT 2022 code 07_DG_2022_05 to P.C. G.R. was supported by the Italian Ministry of Health “Ricerca Corrente”. The work was supported by grants from the Ateneo Project (Sapienza University)”, grant n° RM11916B84D24429 to E.P.