Prader-Willi syndrome (PWS) is a paternally imprinted disorder that leads to sleep, feeding alterations, and temperature instability. It is usually characterized by hypothalamic dysfunctions. Since, the lateral hypothalamus (LH), and its neuronal population, melanin concentrating hormone (MCH) and orexin/hypocretin (OX) neurons are strongly implicated in the regulation of sleep-wake cycle and feeding behavior, we postulate that MCH and OX represent a key component in the pathophysiology of PWS. Specifically, we hypothesized that MCH and OX neurons do not function correctly in the PWS.
In order to test this hypothesis, we designed a three-step research strategy:
1) observational approach:neuronal activity of the LH and its neuronal population (i.e MCH and OX neurons) will be assessed in mice lacking the Snord116gene.
2) functional approach:the role of Snord116 in the control of MCH and OX neuronal functions will be investigated by using gene modification technology
3) interventional approach:manipulation of MCH and OX by pharmacological approach will be performed.
By clarifying the role in of the LH and the two neuronal populations in PWS, we will pave the way for a rescue of the sleep-wake and feed abnormalities.
Prizes and Awards
I was awarded the session on basic neurology at the 2nd Congress of the European Academy of Neurology. 26-31 May 2016 Copenhagen, Denmark “Role of REM sleep and melanin-concentrating hormone in the neuroprotective effect of sleep deprivation pre-ischemia preconditioning”
I was awarded a European Sleep Research Society (ESRS) Travel Grant for Early Career Researchers: at the laboratory of Prof. Pierre-Hervé Luppi, Faculté de Médecine Laënnec, Lyon, France (2014)