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What can we learn from PWS and SNORD116 genes about the pathophysiology of addictive disorders?

Molecular Psychiatry volume 26, pages 51–59 (2021)Cite this article

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Abstract

Addictive disorders have been much investigated and many studies have underlined the role of environmental factors such as social interaction in the vulnerability to and maintenance of addictive behaviors. Research on addiction pathophysiology now suggests that certain behavioral disorders are addictive, one example being food addiction. Yet, despite the growing body of knowledge on addiction, it is still unknown why only some of the individuals exposed to a drug become addicted to it. This observation has prompted the consideration of genetic heritage, neurodevelopmental trajectories, and gene-environment interactions in addiction vulnerability. Prader–Willi syndrome (PWS) is a rare neurodevelopmental disorder in which children become addicted to food and show early social impairment. PWS is caused by the deficiency of imprinted genes located on the 15q11–q13 chromosome. Among them, the SNORD116 gene was identified as the minimal gene responsible for the PWS phenotype. Several studies have also indicated the role of the Snord116 gene in animal and cellular models to explain PWS pathophysiology and phenotype (including social impairment and food addiction). We thus present here the evidence suggesting the potential involvement of the SNORD116 gene in addictive disorders.

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Fig. 1: Representation of the major maternally imprinted genes in the 15q11-q13 chromosomal Prader-Willi region.
Fig. 2: Representation of the common dysfunctions implicated in Prader-Willi Syndrome and addictive disorders and the proposed mechanisms of action of the SNORD116 gene.

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Funding

This work was supported by a grant from the French Association for Prader–Willi syndrome (grant R15062BB).

Author information

Authors and Affiliations

  1. Université de Toulouse III, F-31000, Toulouse, France

    Juliette Salles, Nicolas Franchitto & Maithé Tauber

  2. CHU de Toulouse, Service de psychiatrie et psychologie, psychiatrie Toulouse, F-31000, Toulouse, France

    Juliette Salles

  3. Inserm Unité 1043, CNRS 5828, Université Paul Sabatier, Toulouse III, F-31000, Toulouse, France

    Juliette Salles, Emmanuelle Lacassagne, Sanaa Eddiry, Jean-Pierre Salles & Maithé Tauber

  4. CHU de Toulouse, Institut des Handicaps Neurologiques, Psychiatriques et Sensoriels, F-31000, Toulouse, France

    Juliette Salles & Maithé Tauber

  5. CHU de Toulouse, Service d’addictologie clinique, urgences réanimation médecine, F-31000, Toulouse, France

    Nicolas Franchitto

  6. CHU de Toulouse, Centre de référence du Syndrome de Prader–Willi et autres syndromes avec troubles du comportement alimentaire, Unité d’endocrinologie, obésités, maladies osseuses, génétique et gynécologie médicale, F-31000, Toulouse, France

    Maithé Tauber

Authors
  1. Juliette Salles
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  2. Emmanuelle Lacassagne
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  3. Sanaa Eddiry
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  4. Nicolas Franchitto
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  5. Jean-Pierre Salles
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  6. Maithé Tauber
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Correspondence to Maithé Tauber.

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Salles, J., Lacassagne, E., Eddiry, S. et al. What can we learn from PWS and SNORD116 genes about the pathophysiology of addictive disorders?. Mol Psychiatry 26, 51–59 (2021). https://doi.org/10.1038/s41380-020-00917-x

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  • DOI: https://doi.org/10.1038/s41380-020-00917-x

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