Microglial Endocannabinoid Signalling in AD

被引：16

作者：

Scipioni, Lucia ^{[1
,2
]}

Ciaramellano, Francesca ^{[2
,3
]}

Carnicelli, Veronica ^{[1
]}

Leuti, Alessandro ^{[2
,4
]}

Lizzi, Anna Rita ^{[1
]}

De Dominicis, Noemi ^{[1
,4
]}

Oddi, Sergio ^{[2
,3
]}

Maccarrone, Mauro ^{[1
,2
]}

机构：

[1] Univ Aquila, Dept Biotechnol & Appl Clin Sci, Via Vetoio Snc, I-67100 Laquila, Italy

[2] IRCCS Santa Lucia Fdn, European Ctr Brain Res, Via Fosso di Fiorano 64, I-00143 Rome, Italy

[3] Univ Teramo, Fac Vet Med, Via R Balzarini 1, I-64100 Teramo, Italy

[4] Campus Biomed Univ Rome, Dept Med, Via Alvaro del Portillo 21, I-00128 Rome, Italy

来源：

CELLS | 2022年 / 11卷 / 07期

关键词：

endocannabinoid; microglia; Alzheimer's disease; neuroinflammation; ACID AMIDE HYDROLASE; NLRP3 INFLAMMASOME ACTIVATION; CANNABINOID CB2 RECEPTORS; CENTRAL-NERVOUS-SYSTEM; ALZHEIMERS-DISEASE; MONOACYLGLYCEROL LIPASE; COGNITIVE IMPAIRMENT; AMYLOID PATHOLOGY; NEURONAL SURVIVAL; MOUSE MODEL;

D O I：

10.3390/cells11071237

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Chronic inflammation in Alzheimer's disease (AD) has been recently identified as a major contributor to disease pathogenesis. Once activated, microglial cells, which are brain-resident immune cells, exert several key actions, including phagocytosis, chemotaxis, and the release of pro- or anti-inflammatory mediators, which could have opposite effects on brain homeostasis, depending on the stage of disease and the particular phenotype of microglial cells. The endocannabinoids (eCBs) are pleiotropic bioactive lipids increasingly recognized for their essential roles in regulating microglial activity both under normal and AD-driven pathological conditions. Here, we review the current literature regarding the involvement of this signalling system in modulating microglial phenotypes and activity in the context of homeostasis and AD-related neurodegeneration.

引用

页数：22

共 160 条

[1]

[Anonymous], 2018, ALZHEIMERS DEMENT, DOI DOI 10.1016/J.JALZ.2018.02.001

[2] Role of interleukin 1-beta in the inflammatory response in a fatty acid amide hydrolase-knockout mouse model of Alzheimer's disease [J].