The role of the endocannabinoid system in autism spectrum disorders: Evidence from mouse studies.

Susanna Pietropaolo, Luigi Bellocchio, Inés Bouzón-Arnáiz, Benjamin K. Yee
Progress in Molecular Biology and Translational Science. 2020-01-01; : 183-208
DOI: 10.1016/bs.pmbts.2020.04.016

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Pietropaolo S(1), Bellocchio L(2), Bouzón-Arnáiz I(3), Yee BK(4).

Author information:
(1)University of Bordeaux, Bordeaux Cedex, France; CNRS, INCIA, UMR 5287, Bat
B2, Pessac Cedex, France. Electronic address: .
(2)CNRS, INCIA, UMR 5287, Bat B2, Pessac Cedex, France; INSERM, U1215
NeuroCentre Magendie, Bordeaux Cedex, France.
(3)Institute for Bioengineering of Catalonia (IBEC), The Barcelona Institute of
Science and Technology, Barcelona, Spain; Barcelona Institute for Global Health
(ISGlobal, Hospital Clínic-Universitat de Barcelona), Barcelona, Spain.
(4)Department of Rehabilitation Sciences, Faculty of Health & Social Sciences,
The Hong Kong Polytechnic University, Hong Kong, China.

A substantive volume of research on autism spectrum disorder (ASD) has emerged
in recent years adding to our understanding of the etiopathological process.
Preclinical models in mice and rats have been highly instrumental in modeling
and dissecting the contributions of a multitude of known genetic and
environmental risk factors. However, the translation of preclinical data into
suitable drug targets must overcome three critical hurdles: (i) ASD comprises a
highly heterogeneous group of conditions that can markedly differ in terms of
their clinical presentation and symptoms, (ii) the plethora of genetic and
environmental risk factors suggests a complex, non-unitary, etiopathology, and
(iii) the lack of consensus over the myriad of preclinical models, with respect
to both construct validity and face validity. Against this backdrop, this
Chapter traces how the endocannabinoid system (ECS) has emerged as a promising
target for intervention with predictive validity. Recent supportive preclinical
evidence is summarized, especially studies in mice demonstrating the emergence
of ASD-like behaviors following diverse genetic or pharmacological manipulations
targeting the ECS. The critical relevance of ECS to the complex pathogenesis of
ASD is underscored by its multiple roles in modulating neuronal functions and
shaping brain development. Finally, we argue that important lessons have been
learned from the novel mouse models of ASD, which not only stimulate
game-changing innovative treatments but also foster a consensual framework to
integrate the diverse approaches applied in the search of novel treatments for

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