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Skip to Search Results- 1Beheshti Beglar, Maryam
- 1Devos, Julia J
- 1Eggert, Rachelle
- 1Kamaludin, Ain A
- 1Luck Gibson, Chloe
- 1Tennese, Alysa
- 7Graduate and Postdoctoral Studies (GPS), Faculty of
- 7Graduate and Postdoctoral Studies (GPS), Faculty of/Theses and Dissertations
- 1Concordia University of Edmonton
- 1Concordia University of Edmonton/Independent Research Reports in Undergraduate Biology and Environmental Science (Concordia University of Edmonton)
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Characterizing the Mesolimbic Dopamine Reward Pathway in a Magel2-null Mouse, a Model of Prader-Willi Syndrome
DownloadFall 2016
Prader-Willi Syndrome (PWS) is a genetic disorder characterized by extreme hyperphagia that can lead to severe obesity. The abnormal motivation to eat in PWS suggests a disruption in the hedonic feeding pathway, which is feeding based on reward as opposed to physiological need. Hedonic feeding is...
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Diet Diversity and Health Value in Children with Non-alcoholic Fatty Liver Disease and Prader- Willi Syndrome: Association with Cardio-metabolic Risk
DownloadSpring 2019
In Canada, the obesity prevalence rate in children and adolescents has increased significantly during the last four decades resulting in increased incidence of obesity- related health conditions, lower quality of life and greater health care cost. Patients with non-alcoholic fatty liver disease...
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Inactivation of Magel2 in a mouse model of Prader-Willi Syndrome alters autophagy in the hypothalamus and impairs muscle function
DownloadFall 2016
Prader-Willi Syndrome (PWS) is a neurodevelopmental disorder causing severe neonatal hypotonia that persists until adulthood, reduced muscle mass, and hyperphagia leading to childhood-onset obesity. PWS is caused by inactivation of several genes located on chromosome 15q11-q13, including MAGEL2....
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Investigation of the Prader-Willi syndrome protein MAGEL2 in the regulation of Forkhead box transcription factor FOXO1
DownloadSpring 2013
Prader-Willi syndrome (PWS), a genetic disorder resulting from the loss of expression of multiple genes including MAGEL2, is characterized by hyperphagia and childhood-onset obesity. These symptoms point to dysfunction in the regulation of energy homeostasis. Magel2 is highly expressed in the...
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MAGEL2 regulates leptin receptor internalization through ubiquitination pathways involving USP8 and RNF41
DownloadSpring 2017
Children with Prader-Willi syndrome have neonatal feeding difficulties, developmental delay and excessive appetite. Loss of MAGEL2 alone causes a related neurodevelopmental disorder (Schaaf-Yang syndrome) and may contribute to obesity in children with Prader-Willi syndrome who lack MAGEL2 and...
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2016-11-04
Background: Prader-Willi syndrome (PWS) is a multigene disorder commonly associated with hyperphagia and obesity. Children with PWS have increased fat mass and decreased lean mass before the onset of hyperphagia and obesity. Severe hypotonia and reduced muscle strength are typically present in...
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Fall 2010
Prader-Willi syndrome (PWS) is a rare, neurodevelopmental disorder with multiple features caused by hypothalamic deficiency, including infantile failure to thrive, hyperphagia leading to obesity, growth hormone deficiency, hypogonadism, and central adrenal insufficiency. Other features of PWS...
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The role of the Prader-Willi syndrome obesity protein, MAGEL2 in the proper functioning of circadian rhythm
DownloadFall 2010
MAGEL2 is one of the five genes inactivated in Prader-Willi Syndrome (PWS), a genetic disorder, manifesting with symptoms of developmental delay and morbid obesity. Magel2 is highly expressed in the suprachiasmatic nucleus, which is the location of the central clock or circadian pacemaker. Magel2...