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    Home > Active Ingredient News > Immunology News > Autoantibodies - the body's own antidepressants.

    Autoantibodies - the body's own antidepressants.

    • Last Update: 2020-09-08
    • Source: Internet
    • Author: User
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    If the immune system attacks our own body, it often has devastating consequences: autoantibodies bind to the body, triggering dysfunction.
    glutamate is a neurotransmitter that can also be a target for autoantibodies.
    researchers at the Max Planck Institute for Experimental Medicine in Germany have been studying the circumstances under which autoantibodies targeting a specific glutamate-specific subject (NMDA) are formed and their effects on the brain.
    researchers found that levels of these autoantibodies in the blood fluctuate considerably (not related to health) over a lifetime and increase with age.
    , even early in life, chronic stress can lead to elevated concentrations of these autoantibodies in the blood.
    , when antibodies enter the brain and act on NMDA subjects, depression and anxiety symptoms are reduced, according to the researchers.
    antibodies are clearly the body's own antidepressants.
    NMDA is located on the membrane of nerve cells and binds to the neurotransmitter glutamate.
    it is the type of subject necessary for learning and memory.
    up to 20% of people have antibodies targeting the receptor in their blood.
    , the blood-brain barrier prevents these antibodies from entering the brain from the blood.
    only if the barrier is broken can antibodies have a greater impact.
    if antibodies bind to NMDA subjects in the brain, they are removed (internalized) from the membranes of nerve cells.
    this interferes with signaling to neighboring cells.
    , for example, if inflammation of the brain is caused by a viral infection, the presence of these autoantibodies may lead to so-called "anti-NMDAR encephalitis".
    2016 film Brain on Fire (also translated as My Abnormal Diary) brought public attention to the disease.
    the role of autoantibodies that target NMDA receptors often affects underlying encephalitis symptoms, leading to seizures, movement disorders, mental illness, and loss of cognitive function.
    in this new study, led by Hannelore Ehrenreich of the Max Planck Institute for Experimental Medicine, found that the concentration of these autoantibodies in the blood of mice and humans can fluctuate considerably over time.
    , however, this level increases with age, as the body is constantly exposed to factors that stimulate the immune system, followed by the production of autoantibodies.
    of these factors is stress.
    researchers said autoantibodies to NMDA receptors in the blood of mice exposed to long-term stress were higher than in mice without stress.
    also analyzed the concentration of autoantibodies in the blood of young immigrants.
    Ehrenreich said: "People who are under more stress in their lives are more likely to have autoantibodies in their blood that carry NMDA receptors, even at a young age.
    these autoantibodies are like time bombs in the body.
    if there is an infection or other factor that weakens the blood-brain barrier, autoantibodies can enter the brain and can lead to seizures or other neurological disorders.
    the positive effects of autoantibodies, however, recent research by researchers has shown for the first time that autoantibodies can also play an active role in the brain.
    mice with stronger blood-brain barriers and intra-brain NMDA-like autoantibodies were significantly more mobile and less depressed during long-term stress than their blood-brain counterparts.
    analysis of a large patient database showed that people with NMDA autoantibodies and permeable blood-brain barriers were also significantly less likely to suffer from depression and anxiety.
    NMDA autoantibodies apparently play a similar role in the brain to ketamine, an antidepressant that also acts on NMDA subjects.
    Ehrenreich explains: "The effectiveness of these autoantibodies, whether they cause encephalitis symptoms or suppress depression, obviously depends not only on their level in the brain, but also on any underlying conditions, especially the presence or failure of inflammation.
    " () 
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