The Foundation for Prader-Willi Research announces our first round of Research Awards in 2021 totaling $359,100. FPWR is dedicated to supporting research that advances the understanding and treatment of Prader-Willi syndrome (PWS) and to that end, has awarded over $15,00,000 in research grants since 2003.
On a recent webinar, Dr. Theresa Strong reviewed each of the 4 funded grants, sharing why we're excited about them and what their potential long term contribution could be. You can watch the full 45-minute webinar here or use the links below to watch short 2-minute segments on each specific project.
FPWR PWS Research Grant Recipients, Spring 2021
- REGULATION OF PWS GENES IN THE ENDOCRINE PANCREAS. >Daniel Zeman-Meier, PhD, University of Basel, Switzerland. Pancreatic beta cells produce and secrete two hormones, insulin and amylin, that are important regulators of food intake. These beta cells also express several PWS-region genes, but their function in the pancreas isn’t known. This project will shed light on the role of PWS genes in pancreatic beta cells by studying how PWS genes are regulated in response to cellular signals such as glucose and free fatty acids. The research team will also study the regulation of PWS genes in mouse models that are at risk of developing diabetes. Learn More >>
- HOW IS THE EPITRANSCRIPTOMIC SIGNATURE OF ACTIVE AGRP NEURONS DISRUPTED IN PWS Donna Lehman, PhD, University of Texas Health Science Center. Hyperphagia is thought to be a problem of neurons in the hypothalamus, caused by a dysregulation of neurons that signal being full and being hungry. Disruptions in the code for chemical modifications of RNA (called the epitranscriptome) can have detrimental effects on how neurons function. This project will use human hypothalamic hunger neurons created from stem cells with or without the PWS gene, SNORD116, to provide the first glimpse of how loss of SNORD116 might impact the epitranscriptome. Learn More >>
- ORPHAN GPCRS AND THE NEUROBIOLOGY OF HYPERPHAGIA IN PRADER WILLI SYNDROME: ROLE OF GPR160. Gina Yosten, PhD, Saint Louis University. A protein called CART controls appetite and body weight in both lean and obese rodents and mutations in the CART gene have been linked to obesity in humans. The protein GPR160 helps CART signal brain cells to control appetite. However, CART and GPR160 have not been studied in PWS before. Therefore, this project will evaluate the role of CART in appetite regulation using a rat model of PWS. If this pathway shows promise in PWS, it opens new pathways for PWS treatment. Learn More >>
- COMPARATIVE BEHAVIORAL AND PROTEOMIC ANALYSIS OF RAT SNRPRN AND MAGEL2 MODELS. Rodney Samaco, PhD, Baylor College of Medicine. Two genes disrupted in PWS are SNRPN and MAGEL2, the latter which is the causal gene for Schaaf-Yang syndrome (SYS). The goal of this study is to identify and compare behavioral characteristics and protein profiles of rat models that are deficient for Snrpn and Magel2. These studies will not only provide us a deeper understanding of neurobehavior, organ physiology and changes occurring at the molecular level in these rats, but also provide a great tool for future preclinical studies that may require much needed meaningful biomarkers and outcome measures and will also enable us to identify potential therapeutic interventions. Learn More >>