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Neurotherapeutics. 2015 Oct;12(4):837-47. doi: 10.1007/s13311-015-0371-9.

Endocannabinoid Signaling in Autism.

Author information

1
Centre for Integrative Neuroscience and Neurodynamics, School of Psychology and Clinical Language Sciences, University of Reading, Reading, UK.
2
Center of Integrated Research and School of Medicine, Campus Bio-Medico University of Rome, Via Alvaro del Portillo 21, 00128, Rome, Italy.
3
Mafalda Luce Center for Pervasive Developmental Disorders, Milan, Italy.
4
Faculty of Bioscience and Technology for Food, Agriculture and Environment, University of Teramo, Teramo, Italy.
5
Center of Integrated Research and School of Medicine, Campus Bio-Medico University of Rome, Via Alvaro del Portillo 21, 00128, Rome, Italy. m.maccarrone@unicampus.it.
6
European Center for Brain Research (CERC)/Santa Lucia Foundation, Rome, Italy. m.maccarrone@unicampus.it.

Abstract

Autism spectrum disorder (ASD) is a complex behavioral condition with onset during early childhood and a lifelong course in the vast majority of cases. To date, no behavioral, genetic, brain imaging, or electrophysiological test can specifically validate a clinical diagnosis of ASD. However, these medical procedures are often implemented in order to screen for syndromic forms of the disorder (i.e., autism comorbid with known medical conditions). In the last 25 years a good deal of information has been accumulated on the main components of the "endocannabinoid (eCB) system", a rather complex ensemble of lipid signals ("endocannabinoids"), their target receptors, purported transporters, and metabolic enzymes. It has been clearly documented that eCB signaling plays a key role in many human health and disease conditions of the central nervous system, thus opening the avenue to the therapeutic exploitation of eCB-oriented drugs for the treatment of psychiatric, neurodegenerative, and neuroinflammatory disorders. Here we present a modern view of the eCB system, and alterations of its main components in human patients and animal models relevant to ASD. This review will thus provide a critical perspective necessary to explore the potential exploitation of distinct elements of eCB system as targets of innovative therapeutics against ASD.

KEYWORDS:

Autism spectrum disorder; endocannabinoid system; fragile X syndrome; metabolic regulation; reward system

PMID:
26216231
PMCID:
PMC4604173
DOI:
10.1007/s13311-015-0371-9
[Indexed for MEDLINE]
Free PMC Article

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