Putative neuroprotective actions of N-acyl-ethanolamines

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Putative neuroprotective actions of N-acyl-ethanolamines. / Hansen, Harald S.; Moesgaard, B.; Petersen, G.; Hansen, H.H.

In: Pharmacology & Therapeutics, Vol. 95, No. 2, 01.08.2002, p. 119-126.

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Hansen, HS, Moesgaard, B, Petersen, G & Hansen, HH 2002, 'Putative neuroprotective actions of N-acyl-ethanolamines', Pharmacology & Therapeutics, vol. 95, no. 2, pp. 119-126. https://doi.org/10.1016/S0163-7258(02)00251-6

APA

Hansen, H. S., Moesgaard, B., Petersen, G., & Hansen, H. H. (2002). Putative neuroprotective actions of N-acyl-ethanolamines. Pharmacology & Therapeutics, 95(2), 119-126. https://doi.org/10.1016/S0163-7258(02)00251-6

Vancouver

Hansen HS, Moesgaard B, Petersen G, Hansen HH. Putative neuroprotective actions of N-acyl-ethanolamines. Pharmacology & Therapeutics. 2002 Aug 1;95(2):119-126. https://doi.org/10.1016/S0163-7258(02)00251-6

Author

Hansen, Harald S. ; Moesgaard, B. ; Petersen, G. ; Hansen, H.H. / Putative neuroprotective actions of N-acyl-ethanolamines. In: Pharmacology & Therapeutics. 2002 ; Vol. 95, No. 2. pp. 119-126.

Bibtex

@article{951280ef0ac1462a956d694d086e5b26,
title = "Putative neuroprotective actions of N-acyl-ethanolamines",
abstract = "N-Acyl-ethanolamines (NAEs) and their precursors, N-acyl-ethanolamine phospholipids (NAPEs), are present in the mammalian brain at levels of a few hundred picomoles/gram tissue and a few nanomoles/gram tissue, respectively. NAE-containing arachidonic acid is called anandamide, and it has attracted particular attention since it is a partial agonist for the cannabinoid receptors, for which 2-arachidonoylglycerol is the full agonist. In addition, anandamide may also activate the vanilloid receptor. Anandamide usually amounts to 1-10% of NAEs, as the vast majority of N-acyl groups are saturated and monounsaturated fatty acids. Formation of NAPE and NAE is catalyzed by an N-acyltransferase and an NAPE-hydrolyzing phospholipase D, respectively, two enzymes that have been characterized only preliminary. Interestingly, NAPEs and NAEs accumulate in the brain in response to neurodegenerative insults at a time when other phospholipids are subjected to rapid degradation. This is an important biosynthetic aspect of NAPE and NAE, as NAEs may be neuroprotective by a number of different mechanisms involving both receptor activation and non-receptor-mediated effects, e.g. by binding to cannabinoid receptors and interfering with ceramide turnover, respectively.",
author = "Hansen, {Harald S.} and B. Moesgaard and G. Petersen and H.H. Hansen",
year = "2002",
month = aug,
day = "1",
doi = "10.1016/S0163-7258(02)00251-6",
language = "English",
volume = "95",
pages = "119--126",
journal = "Pharmacology and Therapeutics, Part A: Chemotherapy, Toxicology and",
issn = "0163-7258",
publisher = "Elsevier",
number = "2",

}

RIS

TY - JOUR

T1 - Putative neuroprotective actions of N-acyl-ethanolamines

AU - Hansen, Harald S.

AU - Moesgaard, B.

AU - Petersen, G.

AU - Hansen, H.H.

PY - 2002/8/1

Y1 - 2002/8/1

N2 - N-Acyl-ethanolamines (NAEs) and their precursors, N-acyl-ethanolamine phospholipids (NAPEs), are present in the mammalian brain at levels of a few hundred picomoles/gram tissue and a few nanomoles/gram tissue, respectively. NAE-containing arachidonic acid is called anandamide, and it has attracted particular attention since it is a partial agonist for the cannabinoid receptors, for which 2-arachidonoylglycerol is the full agonist. In addition, anandamide may also activate the vanilloid receptor. Anandamide usually amounts to 1-10% of NAEs, as the vast majority of N-acyl groups are saturated and monounsaturated fatty acids. Formation of NAPE and NAE is catalyzed by an N-acyltransferase and an NAPE-hydrolyzing phospholipase D, respectively, two enzymes that have been characterized only preliminary. Interestingly, NAPEs and NAEs accumulate in the brain in response to neurodegenerative insults at a time when other phospholipids are subjected to rapid degradation. This is an important biosynthetic aspect of NAPE and NAE, as NAEs may be neuroprotective by a number of different mechanisms involving both receptor activation and non-receptor-mediated effects, e.g. by binding to cannabinoid receptors and interfering with ceramide turnover, respectively.

AB - N-Acyl-ethanolamines (NAEs) and their precursors, N-acyl-ethanolamine phospholipids (NAPEs), are present in the mammalian brain at levels of a few hundred picomoles/gram tissue and a few nanomoles/gram tissue, respectively. NAE-containing arachidonic acid is called anandamide, and it has attracted particular attention since it is a partial agonist for the cannabinoid receptors, for which 2-arachidonoylglycerol is the full agonist. In addition, anandamide may also activate the vanilloid receptor. Anandamide usually amounts to 1-10% of NAEs, as the vast majority of N-acyl groups are saturated and monounsaturated fatty acids. Formation of NAPE and NAE is catalyzed by an N-acyltransferase and an NAPE-hydrolyzing phospholipase D, respectively, two enzymes that have been characterized only preliminary. Interestingly, NAPEs and NAEs accumulate in the brain in response to neurodegenerative insults at a time when other phospholipids are subjected to rapid degradation. This is an important biosynthetic aspect of NAPE and NAE, as NAEs may be neuroprotective by a number of different mechanisms involving both receptor activation and non-receptor-mediated effects, e.g. by binding to cannabinoid receptors and interfering with ceramide turnover, respectively.

UR - http://www.scopus.com/inward/record.url?scp=0036669495&partnerID=8YFLogxK

U2 - 10.1016/S0163-7258(02)00251-6

DO - 10.1016/S0163-7258(02)00251-6

M3 - Journal article

AN - SCOPUS:0036669495

VL - 95

SP - 119

EP - 126

JO - Pharmacology and Therapeutics, Part A: Chemotherapy, Toxicology and

JF - Pharmacology and Therapeutics, Part A: Chemotherapy, Toxicology and

SN - 0163-7258

IS - 2

ER -

ID: 45563542