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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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Fall 2014
An individual’s body weight is tightly regulated by balancing food intake with energy expenditure. This is accomplished in part by secretion of the hormone leptin by adipocytes, an excess of which signals to reduce appetite and increase activity through action in the hypothalamic region of the...
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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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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...