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• W1965526018 abstract "Endocannabinoids are bioactive fatty acid amides and esters that play various roles in both the central nervous system and the peripheral nervous system [ 1 Maccarrone M. Finazzi-Agricò A. Endocannabinoids and their actions. Vitam. Horm. 2002; 65: 225-255 Crossref PubMed Google Scholar ]. Anandamide [N-arachidonoylethanolamine (AEA); from ‘ananda’, the Sanskrit word for ‘bliss’] is, together with 2-arachidonoylglycerol, one of the best-studied endocannabinoids. The biological activity of AEA at type-1 and type-2 cannabinoid receptors (CB1 and CB2) is terminated through degradation, which occurs by means of an AEA membrane transporter (AMT) and of an AEA hydrolase [fatty acid amide hydrolase (FAAH); EC 3.5.1.4] [ 2 Bracey M.H. et al. Structural adaptations in a membrane enzyme that terminates endocannabinoid signaling. Science. 2002; 298: 1793-1796 Crossref PubMed Scopus (435) Google Scholar ]. Growing evidence over the past two years has suggested that FAAH is a key regulator of AEA tone and signaling in vivo, and that it might be a suitable target for the therapy of infertility, cancer and neurodegenerative disorders such as Parkinson's disease, Huntington's disease and multiple sclerosis [ 1 Maccarrone M. Finazzi-Agricò A. Endocannabinoids and their actions. Vitam. Horm. 2002; 65: 225-255 Crossref PubMed Google Scholar , 3 Mechoulam R. et al. Cannabinoids and brain injury: therapeutic implications. Trends Mol. Med. 2002; 8: 58-61 Abstract Full Text Full Text PDF PubMed Scopus (212) Google Scholar , 4 Bisogno T. et al. Fatty acid amide hydrolase, an enzyme with many bioactive substrates. Possible therapeutic implications. Curr. Pharm. Des. 2002; 8: 533-547 Crossref PubMed Scopus (106) Google Scholar , 5 Cravatt B.J. Lichtman A.H. Fatty acid amide hydrolase: an emerging therapeutic target in the endocannabinoid system. Curr. Opin. Chem. Biol. 2003; 7: 469-475 Crossref PubMed Scopus (269) Google Scholar ]. In particular, blockade of AEA hydrolysis by FAAH has been shown to reduce anxiety, indicating that FAAH inhibition might also be an innovative approach to anti-anxiety therapy of synthetic compounds – of which URB597 is the most potent – that display unprecedented target selectivity and biological availability [ 6 Kathuria S. et al. Modulation of anxiety through blockade of anandamide hydrolysis. Nat. Med. 2003; 9: 76-817 Crossref PubMed Scopus (1221) Google Scholar ]. In a recent issue of Trends in Molecular Medicine, Gaetani and colleagues discussed the therapeutic implications of these new anti-anxiety drugs in the control of emotional states [ 7 Gaetani S. et al. Anandamide hydrolysis: a new target for anti-anxiety drugs?. Trends Mol. Med. 2003; 28: 474-478 Abstract Full Text Full Text PDF Scopus (98) Google Scholar ] and, potentially, in those disorders whose onset or symptoms are associated with defective production or excessive degradation of AEA and its congeners. Here, I would like to draw attention to the ability of cells to produce their own FAAH inhibitors using a biochemical pathway such as AEA oxygenation catalyzed by lipoxygenase activity, which appears to be a simpler approach to that of the organic chemistry required to synthesize magic bullets such as URB597." @default.
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• W1965526018 date "2004-01-01" @default.
• W1965526018 modified "2023-09-25" @default.
• W1965526018 title "Inhibition of anandamide hydrolysis: cells also know how to do it" @default.
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• W1965526018 doi "https://doi.org/10.1016/j.molmed.2003.11.008" @default.
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