Journal
EXPERIMENTAL NEUROLOGY
Volume 224, Issue 1, Pages 74-84Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.expneurol.2010.03.025
Keywords
Cytokines; Endocannabinoids; Gila; gp120; HAD; HIV-1; Immune surveillance; Neuroinflammation; Neuroprotection; Signal transduction
Categories
Funding
- Fondazione Cassa di Risparmio di Teramo [2009-2012]
- University of Rome Tor Vergata
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Endocannabinoids (eCBs) include a group of lipid mediators that act as endogenous agonists at cannabinoid (CB1, CB2) and vanilloid (TRPV1) receptors. In the last two decades a number of eCBs-metabolizing enzymes have been discovered that, together with eCBs and congeners, target receptors and proteins responsible for their transport and intracellular trafficking form the so-called endocannabinoid system (ECS). Within the central nervous system ECS elements participate in neuroprotection against neuroinflammatory/neurodegenerative diseases like Alzheimer's disease, Parkinson's disease, Huntington's disease, amyotrophic lateral sclerosis, and multiple sclerosis. More recently, a role for eCBs has been documented also in human immunodeficiency virus-1 (HIV-1) envelope glycoprotein gp120-mediated insults, and in HIV-associated dementia (HAD). The modulation of ECS in the latter disease conditions is the subject of this review, that will also address the molecular mechanisms underlying the neuroprotective effects of eCBs. In particular, the interactions between neurons and glia during neuroinflammation, and the alterations of ECS in these cells upon gp120 insults and HAD will be discussed, along with the potential therapeutic exploitation of ECS-oriented drugs for the treatment of HAD and related disorders. (C) 2010 Elsevier Inc. All rights reserved.
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