Signaling pathways in the cerebellum, rather than the hypothalamus, could provide a key for developing new therapies for the genetic disorder.
What to know:
Disordered signaling in the cerebellum may help explain the insatiable appetite experienced by people with Prader-Willi Syndrome (PWS), according to new research led by J. Nicholas Betley, PhD, at the University of Pennsylvania in Philadelphia.
Previous studies have shown that neural circuits in the hindbrain and hypothalamus help regulate food intake, but drugs targeting these regions to help patients with obesity have met with limited success.
Comparing functional MRI scans of patients with PWS and those without the disorder, Betley’s team observed differences in how the cerebellum region responded to food in each group.
In a subsequent study in mice, allegra vs claritin 2014 the researchers observed that neurons in the cerebellum’s anterior deep cerebellar nuclei (aDCN) were shown to activate after eating. Activating the neurons in the aDCN resulted in the mice constraining how much they ate, while inhibiting them caused the mice to eat more.
The activated aDCN neurons were also associated with dopamine levels, suggesting a complex relationship with the feeling of “reward” from eating that could point toward future therapies.
This is a summary of the article “In the brain’s cerebellum, a new target for suppressing hunger” published by the University of Pennsylvania on November 17. The full article can be found on penntoday.upenn.com.
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