It is always rewarding to see the impact that FPWR funds have on helping researchers advance projects and publish in the scientific literature! Four recent papers supported by FPWR are highlighted below.
The PWS community and FPWR are very fortunate to work in collaboration with a number of talented researchers who are dedicated to better understanding PWS and to helping us meet our mission of eliminating the challenges of PWS through the advancement of research. One of these researchers is Dr. Andrea Haqq at the University of Alberta. Dr.
FPWR continues to energize the field of PWS research! Our most recent funding cycle received almost 30 applications from researchers around the world. The bulk of this grant cycle was composed of applications to the general grants program, covering a broad range of research questions as diverse as the many aspects of PWS, from basic molecular and genetic studies to clinical interventions. In addition, this grant cycle also included a special request for applications targeted towards the understudied questions and impact of mental health in PWS.
Objective: PYY3-36 and PP potently inhibit food intake in rodents and humans, however, it is unclear whether they have any synergistic/additive interaction in decreasing food intake. Design and Methods: Fasted WT, Y2-/- , Y4-/- or Y2Y4-/- mice were i.p. administrated with saline, PYY3-36 and/or PP. Results: We demonstrate that combined injection of PYY3-36 and PP reduces food intake in an additive manner. This effect is mediated via Y2 and Y4 receptors, respectively.
Prader-Willi Syndrome (PWS) is a genetic disease characterized by failure to thrive and low muscle tone during infancy, followed by food-seeking, insatiable appetite and progressive obesity in childhood. The resulting increases in total body fat and decreases in muscle mass lead to metabolic problems such as diabetes and heart disease. Several diets are recommended for the management of body weight in individuals with PWS such as the Red-Yellow-Green system which is a low-fat, low calorie diet.
In a recent email correspondence, Dr. Cunningham at the University of Texas Medical Branch thanked FPWR and described the contribution that FPWR grant funds (2010-2011) have had on the work coming out of her laboratory. She writes, "thank you for the support which allowed us to build an entirely new program to develop therapeutics for those affected by PWS...We have made incredible progress on this research program, thanks in great part for the support from the FPWR.
Here's a blog from FPWR Board member Shawn Johnson about the "PWS Research Challenge: Advancing Appetite and Satiety Research", which FPWR has launched in collaboration with InnoCentive. Shawn championed the idea of a crowdsourcing approach to generate new insight into hyperphagia in PWS:
Prader-Willi syndrome (PWS) is a disease caused by mutations on human chromosome 15 leading to "floppy" infants initially, and obesity and sleep disorders later. Although genetic defects underlying PWS have been documented, it is still not well understood how the loss-of-function of genes results in various symptoms in PWS. It has been shown that the dysfunction of the hypothalamus, a brain structure, contributes to symptoms seen in PWS patients.
Prader-Willi Syndrome (PWS) is a complex genetic disorder in which several genes are missing or not functional. PWS is characterized by initial loss of muscle tone and failure to thrive neonatally; children with PWS develop behavioral and cognitive problems, reproductive defects, and excessive overeating. A major medical concern is the morbid obesity that results from incessant food-seeking and an inability to feel full. The chromosomal defect in PWS patients deletes a gene sequence involved in regulating a receptor found in the brain, the serotonin 5-HT2C receptor (5-HT2CR).