Anti-Inflammatory Effects of Fatty Acid Amide Hydrolase Inhibition in Monocytes/Macrophages from Alzheimer's Disease Patients.
Aged
Alzheimer Disease
/ pathology
Amidohydrolases
/ antagonists & inhibitors
Benzamides
/ pharmacology
Carbamates
/ pharmacology
Female
Humans
Interleukin-6
/ metabolism
Leukocytes, Mononuclear
/ cytology
Lipopolysaccharides
/ pharmacology
Macrophages
/ cytology
Male
Middle Aged
Receptor, Cannabinoid, CB1
/ metabolism
Receptor, Cannabinoid, CB2
/ metabolism
Tumor Necrosis Factor-alpha
/ metabolism
Alzheimer’s disease
cytokines
fatty acid amide hydrolase
immunomodulation
monocytes/macrophages
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
26 03 2021
26 03 2021
Historique:
received:
21
01
2021
revised:
19
03
2021
accepted:
23
03
2021
entrez:
3
4
2021
pubmed:
4
4
2021
medline:
18
9
2021
Statut:
epublish
Résumé
Growing evidence shows that the immune system is critically involved in Alzheimer's disease (AD) pathogenesis and progression. The modulation and targeting of peripheral immune mechanisms are thus promising therapeutic or preventive strategies for AD. Given the critical involvement of the endocannabinoid (eCB) system in modulating immune functions, we investigated the potential role of the main elements of such a system, namely type-1 and type-2 cannabinoid receptors (CB
Identifiants
pubmed: 33810505
pii: biom11040502
doi: 10.3390/biom11040502
pmc: PMC8066292
pii:
doi:
Substances chimiques
Benzamides
0
Carbamates
0
Interleukin-6
0
Lipopolysaccharides
0
Receptor, Cannabinoid, CB1
0
Receptor, Cannabinoid, CB2
0
Tumor Necrosis Factor-alpha
0
cyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl ester
0
Amidohydrolases
EC 3.5.-
fatty-acid amide hydrolase
EC 3.5.1.-
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Références
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