ReviewJournal of neuroendocrinology2021
Hypothalamic neuropeptides and neurocircuitries in Prader Willi syndrome.
Review in Journal of neuroendocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Intranasal Carbetocin Reduces Hyperphagia, Anxiousness, and Distress in Prader-Willi Syndrome: CARE-PWS Phase 3 Trial.The Journal of clinical endocrinology and metabolism · 2023Trial
- Child with genetically confirmed Prader-Willi syndrome.BMJ case reports · 2026Article
- Tanycyte BMAL1 regulates high-fat diet weight gain and shapes arcuate neurogenesis in female mice.Cell reports · 2026Article
- Neuropeptides and the Autonomic Nervous System in Prader-Willi Syndrome.International journal of molecular sciences · 2025Review
- Selective changes in vasopressin neurons and astrocytes in the suprachiasmatic nucleus of Prader-Willi syndrome subjects.Journal of neuroendocrinology · 2025Article
- The Role of the Arcuate Nucleus in Regulating Hunger and Satiety in Prader-Willi Syndrome.Current issues in molecular biology · 2025Review
- Differential DNA methylation in iPSC-derived dopaminergic neurons: a step forward on the role of SNORD116 microdeletion in the pathophysiology of addictive behavior in Prader-Willi syndrome.Molecular psychiatry · 2024Article
- Microglial phagolysosome dysfunction and altered neural communication amplify phenotypic severity in Prader-Willi Syndrome with larger deletion.Acta neuropathologica · 2024Article
- AAV-BDNF gene therapy ameliorates a hypothalamic neuroinflammatory signature in theMolecular therapy. Methods & clinical development · 2023Article
- Hormonal Imbalances in Prader-Willi and Schaaf-Yang Syndromes Imply the Evolution of Specific Regulation of Hypothalamic Neuroendocrine Function in Mammals.International journal of molecular sciences · 2023Review
- Circulating Levels of Nesfatin-1 and Spexin in Children with Prader-Willi Syndrome during Growth Hormone Treatment and Dietary Intervention.Nutrients · 2023Article
- Progress in Brain Magnetic Resonance Imaging of Individuals with Prader-Willi Syndrome.Journal of clinical medicine · 2023Review
- Prader-Willi syndrome: Symptoms and topiramate response in light of genetics.Frontiers in neuroscience · 2023Article
- Linking oxytocin and arginine vasopressin signaling abnormalities to social behavior impairments in Prader-Willi syndrome.Neuroscience and biobehavioral reviews · 2022Review
- Reference Genes across Nine Brain Areas of Wild Type and Prader-Willi Syndrome Mice: Assessing Differences inInternational journal of molecular sciences · 2022Article
- Distinct promoter regions of the oxytocin receptor gene are hypomethylated in Prader-Willi syndrome and in Prader-Willi syndrome associated psychosis.Translational psychiatry · 2022Article
- Hypothalamic syndrome.Nature reviews. Disease primers · 2022Review
- Sleep-disordered breathing in school-aged children with Prader-Willi syndrome.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2022Article
- Neurobehavioral Dimensions of Prader Willi Syndrome: Relationships Between Sleep and Psychosis-Risk Symptoms.Frontiers in psychiatry · 2022Article
- Alteration of brain nuclei in obese children with and without Prader-Willi syndrome.Frontiers in neuroinformatics · 2022Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Prader-Willi Syndrome (PWS) is a rare and incurable congenital neurodevelopmental disorder, resulting from the absence of expression of a group of genes on the paternally acquired chromosome 15q11-q13. Phenotypical characteristics of PWS include infantile hypotonia, short stature, incomplete pubertal development, hyperphagia and morbid obesity. Hypothalamic dysfunction in controlling body weight and food intake is a hallmark of PWS. Neuroimaging studies have demonstrated that PWS subjects have abnormal neurocircuitry engaged in the hedonic and physiological control of feeding behavior. This is translated into diminished production of hypothalamic effector peptides which are responsible for the coordination of energy homeostasis and satiety. So far, studies with animal models for PWS and with human post-mortem hypothalamic specimens demonstrated changes particularly in the infundibular and the paraventricular nuclei of the hypothalamus, both in orexigenic and anorexigenic neural populations. Moreover, many PWS patients have a severe endocrine dysfunction, e.g. central hypogonadism and/or growth hormone deficiency, which may contribute to the development of increased fat mass, especially if left untreated. Additionally, the role of non-neuronal cells, such as astrocytes and microglia in the hypothalamic dysregulation in PWS is yet to be determined. Notably, microglial activation is persistently present in non-genetic obesity. To what extent microglia, and other glial cells, are affected in PWS is poorly understood. The elucidation of the hypothalamic dysfunction in PWS could prove to be a key feature of rational therapeutic management in this syndrome. This review aims to examine the evidence for hypothalamic dysfunction, both at the neuropeptidergic and circuitry levels, and its correlation with the pathophysiology of PWS.
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Registered trials
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.