Grants and Contracts Details
Description
One of the most severe daily problems in Prader-Willi syndrome (PWS) is the inability to reach satiety
after a meal, which leads to hyperphagia and obesity. The loss of expression of two small nucleolar RNA
(snoRNA) clusters is a crucial genetic contributor to the disease. One of these snoRNAs (SNORD115)
promotes the most active form of the serotonin receptor 2C (HTR2C). Activated HTR2C receptors in the
arcuate nucleus inhibit food uptake. We developed an oligonucleotide (“oligo#5”) that similar to
SNORD115 promotes the formation of the most active HTR2C receptor that localizes on the cell surface.
Oligo#5 inhibits food uptake of fasted mice when delivered by intracerebroventricular (ICV) injection to
the arcuate nucleus. We postulate that oligo#5 could be developed into an anti hyperphagia drug for
Prader-Willi syndrome.
Status | Finished |
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Effective start/end date | 9/23/14 → 8/31/17 |
Funding
- National Institute of Child Health and Human Develop: $408,546.00
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