Macamides As Potential Therapeutic Agents in Neurological Disorders

Overview

Journal Neurol Int

Publisher MDPI

Specialty Neurology

Date 2024 Nov 25

PMID 39585076

Authors

Karin J Vera-Lopez

Gonzalo Davila-Del-Carpio

Rita Nieto-Montesinos

Affiliations

Soon will be listed here.

Abstract

Therapeutic treatment of nervous system disorders has represented one of the significant challenges in medicine for the past several decades. Technological and medical advances have made it possible to recognize different neurological disorders, which has led to more precise identification of potential therapeutic targets, in turn leading to research into developing drugs aimed at these disorders. In this sense, recent years have seen an increase in exploration of the therapeutic effects of various metabolites extracted from Maca (Lepidium meyenii), a plant native to the central alpine region of Peru. Among the most important secondary metabolites contained in this plant are macamides, molecules derived from N-benzylamides of long-chain fatty acids. Macamides have been proposed as active drugs to treat some neurological disorders. Their excellent human tolerance and low toxicity along with neuroprotective, immune-enhancing, and and antioxidant properties make them ideal for exploration as therapeutic agents. In this review, we have compiled information from various studies on macamides, along with theories about the metabolic pathways on which they act.

Citing Articles

Anticonvulsant Effects of Synthetic -(3-Methoxybenzyl)oleamide and -(3-Methoxybenzyl)linoleamide Macamides: An In Silico and In Vivo Study.

Vera-Lopez K, Aguilar-Pineda J, Moscoso-Palacios R, Davila-Del-Carpio G, Manrique-Murillo J, Gomez B Molecules. 2025; 30(2).

PMID: 39860203 PMC: 11767965. DOI: 10.3390/molecules30020333.

References

Benito C, Romero J, Tolon R, Clemente D, Docagne F, Hillard C . Cannabinoid CB1 and CB2 receptors and fatty acid amide hydrolase are specific markers of plaque cell subtypes in human multiple sclerosis. J Neurosci. 2007; 27(9):2396-402. PMC: 6673484. DOI: 10.1523/JNEUROSCI.4814-06.2007. View

Devane W, Dysarz 3rd F, Johnson M, Melvin L, Howlett A . Determination and characterization of a cannabinoid receptor in rat brain. Mol Pharmacol. 1988; 34(5):605-13. View

Brodie M, Besag F, Ettinger A, Mula M, Gobbi G, Comai S . Epilepsy, Antiepileptic Drugs, and Aggression: An Evidence-Based Review. Pharmacol Rev. 2016; 68(3):563-602. PMC: 4931873. DOI: 10.1124/pr.115.012021. View

Wang X, Wang W, Li L, Perry G, Lee H, Zhu X . Oxidative stress and mitochondrial dysfunction in Alzheimer's disease. Biochim Biophys Acta. 2013; 1842(8):1240-7. PMC: 4007397. DOI: 10.1016/j.bbadis.2013.10.015. View

Gainetdinov R, Premont R, Bohn L, Lefkowitz R, Caron M . Desensitization of G protein-coupled receptors and neuronal functions. Annu Rev Neurosci. 2004; 27:107-44. DOI: 10.1146/annurev.neuro.27.070203.144206. View

Howlett A, Abood M . CB and CB Receptor Pharmacology. Adv Pharmacol. 2017; 80:169-206. PMC: 5812699. DOI: 10.1016/bs.apha.2017.03.007. View

Apostolova L . Alzheimer Disease. Continuum (Minneap Minn). 2016; 22(2 Dementia):419-34. PMC: 5390933. DOI: 10.1212/CON.0000000000000307. View

Beharry S, Heinrich M . Is the hype around the reproductive health claims of maca (Lepidium meyenii Walp.) justified?. J Ethnopharmacol. 2017; 211:126-170. DOI: 10.1016/j.jep.2017.08.003. View

Mori A . How do adenosine A receptors regulate motor function?. Parkinsonism Relat Disord. 2020; 80 Suppl 1:S13-S20. DOI: 10.1016/j.parkreldis.2020.09.025. View

10.

Yi F, Tan X, Yan X, Liu H . In silico profiling for secondary metabolites from (maca) by the pharmacophore and ligand-shape-based joint approach. Chin Med. 2016; 11:42. PMC: 5037646. DOI: 10.1186/s13020-016-0112-y. View

11.

Chong F, Ng K, Koh R, Chye S . Tau Proteins and Tauopathies in Alzheimer's Disease. Cell Mol Neurobiol. 2018; 38(5):965-980. PMC: 11481908. DOI: 10.1007/s10571-017-0574-1. View

12.

Domenici M, Ferrante A, Martire A, Chiodi V, Pepponi R, Tebano M . Adenosine A receptor as potential therapeutic target in neuropsychiatric disorders. Pharmacol Res. 2019; 147:104338. DOI: 10.1016/j.phrs.2019.104338. View

13.

Yu Z, Jin W, Cui Y, Ao M, Liu H, Xu H . Protective effects of macamides from Walp. against corticosterone-induced neurotoxicity in PC12 cells. RSC Adv. 2022; 9(40):23096-23108. PMC: 9067313. DOI: 10.1039/c9ra03268a. View

14.

Yang D, Zhou Q, Labroska V, Qin S, Darbalaei S, Wu Y . G protein-coupled receptors: structure- and function-based drug discovery. Signal Transduct Target Ther. 2021; 6(1):7. PMC: 7790836. DOI: 10.1038/s41392-020-00435-w. View

15.

Wajngarten M, Silva G . Hypertension and Stroke: Update on Treatment. Eur Cardiol. 2019; 14(2):111-115. PMC: 6659031. DOI: 10.15420/ecr.2019.11.1. View

16.

Garcia-Gil M, Camici M, Allegrini S, Pesi R, Tozzi M . Metabolic Aspects of Adenosine Functions in the Brain. Front Pharmacol. 2021; 12:672182. PMC: 8160517. DOI: 10.3389/fphar.2021.672182. View

17.

Tao H, Shi H, Wang M, Xu Y . Macamide B suppresses lung cancer progression potentially via the ATM signaling pathway. Oncol Lett. 2023; 25(3):115. PMC: 9950334. DOI: 10.3892/ol.2023.13701. View

18.

Zverova M . Clinical aspects of Alzheimer's disease. Clin Biochem. 2019; 72:3-6. DOI: 10.1016/j.clinbiochem.2019.04.015. View

19.

Minton O, Richardson A, Sharpe M, Hotopf M, Stone P . A systematic review and meta-analysis of the pharmacological treatment of cancer-related fatigue. J Natl Cancer Inst. 2008; 100(16):1155-66. DOI: 10.1093/jnci/djn250. View

20.

Alasmari M, Bhlke M, Kelley C, Maher T, Pino-Figueroa A . Inhibition of Fatty Acid Amide Hydrolase (FAAH) by Macamides. Mol Neurobiol. 2018; 56(3):1770-1781. DOI: 10.1007/s12035-018-1115-8. View