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    Home > Active Ingredient News > Study of Nervous System > These people never feel full, the problem is in their cerebellum

    These people never feel full, the problem is in their cerebellum

    • Last Update: 2022-02-21
    • Source: Internet
    • Author: User
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    Image source: Article by Pixabay | Diana Kwon Translation | Huang Chen Prader-Willi syndrome is a rare genetic disorder in which people never feel full
    .

    This lack of satiety can lead to severe obesity, which can lead to life-threatening diseases
    .

    Although the fist-sized cerebellum has never been linked to hunger before, scientists have now discovered that the cerebellum plays a key role in regulating satiety in people with Prader-Willi syndrome
    .

    The cerebellum has long been thought to be primarily involved in motor coordination, but this study raises a new perspective — it also plays a broad role in cognition, emotion and behavior
    .
    "We've opened up a whole new area of ​​research into how the cerebellum controls food intake, "
    says Albert Chen, a neuroscientist at the Scintillon Institute in California
    .

    In fact, the research project started with a casual observation
    .

    Chen and team found that when they activated some neurons outside the anterior deep cerebellar nuclei (aDCN) of the mice's deep cerebellar nuclei, the mice stopped eating
    .

    This piqued their interest and subsequently contacted collaborators at Harvard Medical School
    .

    Scientists at Harvard University recruited 14 people with Prader-Willi syndrome and 14 people without the disease to serve as the experimental and control groups for the study, and used functional magnetic resonance imaging (fMRI) to monitor their performance.
    Brain activity when seeing pictures of food at different levels of satiety (just after eating or fasting for more than 4 hours)
    .

    The results of the analysis showed that, in the same brain region that Chen's team found in mice, the brain region of Prader-Willi syndrome patients, the aDCN, showed significant neural activity compared to healthy people.
    exception
    .

    For healthy people, the aDCN after fasting for a period of time was activated after seeing pictures of food compared to just after eating; but for Prader-Willi syndrome patients, the two satiety states There was no significant change in the neural activity of the aDCN when it came to food photos
    .

    This suggests that aDCN is helping us control our appetite and food intake
    .

    To further confirm this, several research institutions conducted more mouse experiments
    .

    It was found that when aDCN neurons in mice were activated, they instead inhibited the activity of neurons that are pleasant to eat, resulting in a significant reduction in food intake
    .

    The related findings were published in the journal Nature
    .

    For many years, neuroscientists' research on appetite has focused on the hypothalamus, or nucleus accumbens, an area of ​​the brain involved in regulating energy balance, and the nucleus accumbens is the core of the brain's reward system
    .

    Elanor Hinton, a neuroscientist at the University of Bristol in the U.
    K.
    , who was not involved in the study, said the latest research has identified a new key region in the brain that regulates eating
    .

    Hinton continued: "I've been doing appetite-related research for the past 15 years or so, but I've never considered a role for the cerebellum
    .

    I think this study looking at the cerebellum is not only useful for treating Prader.
    -Willi's syndrome is very important, and it's very important to address obesity in the general population
    .

    " Now, the researchers plan to test the ability to use a non-invasive intervention technique called Transcranial Magnetic Stimulation in healthy people.
    This neural circuit that controls the brain
    .

    If the test is successful, they hope the technology will eventually make it into clinical trials, Chen said
    .

    Click on the picture or read the original text in the sales of the new issue of "Universal Science" in January.
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