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    Home > Medical News > Medical Science News > The brain's "sober" mechanism helps to find new drug targets

    The brain's "sober" mechanism helps to find new drug targets

    • Last Update: 2021-03-30
    • Source: Internet
    • Author: User
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    The brain's "sober" mechanism helps to find new drug targets
    The brain's sobering mechanism helps to find new drug targets.


    Picture of Zhang Liti on the cover of"Nature-Metabolism"

     "Nature-Metabolism" CoverZhang Liti Picture "Nature-Metabolism" Zhang Liti Picture

    "We used to far underestimate the brain's ability to metabolize alcohol and its impact on drinking behavior.


    In the early morning of March 23, Beijing time, Zhang Li's team published a paper in Nature-Metabolism in the form of a cover article, revealing the function of alcohol metabolism in the brain and new cell-specific brain regions and specific neurochemical mechanisms that cause drunken behavior.


    Found that alcohol is metabolized in the brain

    Found that alcohol is metabolized in the brain

    We usually think that alcohol is mainly metabolized in the liver.


    Ethanol and acetaldehyde are both highly active substances, and they have a great impact on the nervous system, but in the past, people knew little about the relationship between acetic acid and drunken behavior.


    "There is a large amount of ALDH2 in the liver.


    Researchers analyzed the effect of acetic acid on the content of inhibitory neurotransmitter GABA from the electrophysiology of mouse brain slices and multiple levels of single-cell astrocytes.


    "We also unexpectedly observed that the acetic acid transferred from the periphery to the brain has little effect on GABA.


    Especially important for Chinese

    Especially important for Chinese

    As the high-level center of the body, the brain is also very sensitive to the response to alcohol intake.


    As the key enzyme that converts acetaldehyde to acetic acid, ALDH2 is very important.


    Although more than 90% of alcohol is metabolized in the liver after drinking, acetate is formed by acetaldehyde.


    "This suggests that ALDH2 in the brain astrocytes is the main mechanism for alcohol to directly regulate related behavioral damage to the brain.


    Open up new research directions

    Open up new research directions

    This study revealed for the first time that the central mechanism of alcohol metabolism and its induced motor and balance dysfunction are closely related to the function of astrocyte ALDH2 in the cerebellum.


    "Because of the large number of astrocytes, they are easy to be activated and continue to divide.


    In addition, ALDH2 is also involved in the process of regulating the metabolism of various neurotransmitters in the brain and scavenging free radicals.


    The three reviewers of "Nature-Metabolism" unanimously gave high praise to this research.


    "Most research on how alcohol consumption affects human behavior has focused on the effects of ethanol.
    In the past few decades, research on how ethanol changes the central nervous system has made substantial progress.
    This research has established the field of alcohol research.
    A milestone, it provides new clues for a study that has been rarely considered, which regulates the behavioral effects of alcohol in the brain.
    " Nicolas X.
    Tritsch, a professor at the Institute of Neuroscience, New York University School of Medicine, in the same journal The author commented on it.

    "AlDH2 in the brain astrocytes should be an important target for the future treatment of alcoholism, anti-alcoholism, and alcohol dependence.
    " Zhang Li said, "In recent years, the development of new drugs for ALDH2 inhibitors has been active, but these drugs all increase blood pressure.
    Medium acetaldehyde concentration, long-term use can cause cancer.
    In the future, the development of cell-specific ALDH2 inhibitors can be considered.
    ” (Source: Zhang Shuanghu, China Science News)

    Related paper information: org/10.
    1038/s42255-021-00357-z" target="_blank">https://doi.
    org/10.
    1038/s42255-021-00357-z

    org/10.
    1038/s42255-021-00357-z" target="_blank">https://doi.
    org/10.
    1038/s42255-021-00357-z
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