Prader-Willi syndrome (PWS) is a genetic disease characterized by an insatiable appetite and a variety or behavioral dysregulations. It is known that the brain, and particularly a region of the brain called the hypothalamus, is important to regulating appetite and body weight. We also know that many key physiological processes, including appetite regulation, are established during the perinatal period, that time just prior to and soon after birth. We previously found that the development of neurons that cause satiety is attenuated in a mouse model for PWS. Using mouse models, this research project will investigate the specific cellular mechanisms that are responsible for the loss of satiety signals in PWS. We will also test whether intervening with this cellular pathway will ameliorate the nerve cell deficits observed PWS. Understanding of the impairments in the brain cells that cause satiety is critical for designing treatments and cures for PWS. The knowledge we gain from this project may therefore help identify therapeutic targets to reduce the insatiable appetite associated with PWS.
This project is in loving memory of baby Violet Ai Xin Hasenmyer, a life that was lost too soon, but a life that was not without purpose or joy.