ReviewMolecular psychiatry2021
What can we learn from PWS and SNORD116 genes about the pathophysiology of addictive disorders?
Review in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Hyperphagia in Prader-Willi syndrome: linking hypothalamic dysfunction to clinical assessment and management across the lifespan.Orphanet journal of rare diseases · 2026Review
- Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader-Willi syndrome.The Journal of physiology · 2026Article
- Aberrant local and global neural activation patterns in pediatric Prader-Willi syndrome.Frontiers in neuroscience · 2026Article
- Towards a genetic obesity risk score in a single-center study of children and adolescents with obesity.Scientific reports · 2025Article
- Food responsiveness, addiction, and hyperphagia in Prader-Willi syndrome: a cross-sectional study of 210 Chinese patients.Frontiers in endocrinology · 2025Article
- Give me five! A modern perspective on addiction from the up-dated Freudian drive theory.Frontiers in psychiatry · 2025Article
- Roles of SNORD115 and SNORD116 ncRNA clusters during neuronal differentiation.Nature communications · 2024Article
- Small Nucleolar RNAs in Solid Tumors: A Brief Review of the Literature on These Potential Biomarkers.Asian Pacific journal of cancer prevention : APJCP · 2024Review
- SNORA69 is up-regulated in the lateral habenula of individuals with major depressive disorder.Scientific reports · 2024Article
- Progress in Brain Magnetic Resonance Imaging of Individuals with Prader-Willi Syndrome.Journal of clinical medicine · 2023Review
- Food socialization of children with Prader-Willi syndrome: an interdisciplinary problematization.Frontiers in nutrition · 2023Article
- Prader-Willi syndrome: Symptoms and topiramate response in light of genetics.Frontiers in neuroscience · 2023Article
- Amygdala hyperactivation relates to eating behaviour: a potential indicator of food addiction in Prader-Willi syndrome.Brain communications · 2023Article
- Analysis ofGenes · 2022Review
- Approach to the Patient With Prader-Willi Syndrome.The Journal of clinical endocrinology and metabolism · 2022Article
- Impact of Deprivation on Obesity in Children with PWS.Journal of clinical medicine · 2022Article
- Diabetes Mellitus in Prader-Willi Syndrome: Natural History during the Transition from Childhood to Adulthood in a Cohort of 39 Patients.Journal of clinical medicine · 2021Article
- SNORD116 and growth hormone therapy impact IGFBP7 in Prader-Willi syndrome.Genetics in medicine : official journal of the American College of Medical Genetics · 2021Article
- Patients with PWS and related syndromes display differentially methylated regions involved in neurodevelopmental and nutritional trajectory.Clinical epigenetics · 2021Article
- Behavioral features in Prader-Willi syndrome (PWS): consensus paper from the International PWS Clinical Trial Consortium.Journal of neurodevelopmental disorders · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.