ReviewNeurobiology of learning and memory2019
Cognitive deficits in the Snord116 deletion mouse model for Prader-Willi syndrome.
Review in Neurobiology of learning and memory, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
42 citing papers in PubMed, 74 citations in OpenAlex.
- Altered neural electrophysiological properties in the anterior cingulate cortex in a mouse model of Prader-Willi syndrome.The Journal of physiology · 2026Article
- Brain and knee joint degeneration following anterior cruciate ligament injury in a mouse model of Alzheimer's disease.JBMR plus · 2026Article
- Aberrant local and global neural activation patterns in pediatric Prader-Willi syndrome.Frontiers in neuroscience · 2026Article
- Article
- Small Nucleolar RNAs: Biological Functions and Diseases.MedComm · 2025Review
- Investigation of a mouse model of Prader-Willi Syndrome with combined disruption of Necdin and Magel2.JCI insight · 2025Article
- Peptidomimetic inhibitors targeting TrkB/PSD-95 signaling improves cognition and seizure outcomes in an Angelman Syndrome mouse model.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Characterization of Circulating Protein Profiles in Individuals with Prader-Willi Syndrome and Individuals with Non-Syndromic Obesity.Journal of clinical medicine · 2024Article
- Surgical restabilization reduces the progression of post-traumatic osteoarthritis initiated by ACL rupture in mice.Osteoarthritis and cartilage · 2024Article
- SNORA69 is up-regulated in the lateral habenula of individuals with major depressive disorder.Scientific reports · 2024Article
- Coordinated evolution of the SNORD115 and SNORD116 tandem repeats at the imprinted Prader-Willi/Angelman locus.NAR molecular medicine · 2024Article
- The emerging role of snoRNAs in human disease.Genes & diseases · 2023Review
- Linking oxytocin and arginine vasopressin signaling abnormalities to social behavior impairments in Prader-Willi syndrome.Neuroscience and biobehavioral reviews · 2022Review
- Touchscreen cognitive deficits, hyperexcitability and hyperactivity in males and females using two models of Cdkl5 deficiency.Human molecular genetics · 2022Article
- Gait as a quantitative translational outcome measure in Angelman syndrome.Autism research : official journal of the International Society for Autism Research · 2022Article
- Dietary Conjugated Linoleic Acid Reduces Body Weight and Fat inNutrients · 2022Article
- Phylogenetic and Molecular Analyses Identify SNORD116 Targets Involved in the Prader-Willi Syndrome.Molecular biology and evolution · 2022Article
- Excessive Laughter-like Vocalizations, Microcephaly, and Translational Outcomes in theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Insulin-like growth factor-2 does not improve behavioral deficits in mouse and rat models of Angelman Syndrome.Molecular autism · 2021Article
- Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Prader-Willi syndrome (PWS) is an imprinted neurodevelopmental disease caused by a loss of paternal genes on chromosome 15q11-q13. It is characterized by cognitive impairments, developmental delay, sleep abnormalities, and hyperphagia often leading to obesity. Clinical research has shown that a lack of expression of SNORD116, a paternally expressed imprinted gene cluster that encodes multiple copies of a small nucleolar RNA (snoRNA) in both humans and mice, is most likely responsible for many PWS symptoms seen in humans. The majority of previous research using PWS preclinical models focused on characterization of the hyperphagic and metabolic phenotypes. However, a crucial understudied clinical phenotype is cognitive impairments and thus we investigated the learning and memory abilities using a model of PWS, with a heterozygous deletion in Snord116. We utilized the novel object recognition task, which doesn't require external motivation, or exhaustive swim training. Automated findings were further confirmed with manual scoring by a highly trained blinded investigator. We discovered deficits in Snord116+/- mutant mice in the novel object recognition, location memory and tone cue fear conditioning assays when compared to age-, sex- matched, littermate control Snord116+/+ mice. Further, we confirmed that despite physical neo-natal developmental delays, Snord116+/- mice had normal exploratory and motor abilities. These results show that the Snord116+/- deletion murine model is a valuable preclinical model for investigating learning and memory impairments in individuals with PWS without common confounding phenotypes.
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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.