De meest voorname oorzaak van de klachten bij neuroborreliose is de neurotoxine
Quinolinic Acid.
Quinolinic acid has a potent neurotoxic effect. Studies have demonstrated that quinolinic acid may be involved in many psychiatric disorders, neurodegenerative processes in the brain, as well as other disorders. Within the brain, quinolinic acid is only produced by activated microglia and macrophages.
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WikipediaDeze Quinolinic Acid komt overigens niet alleen voor bij Lyme maar ook bij andere infecties van het centraal zenuwstelsel en de hersenen. En deze Quinolinic Acid treffen ze ook in verhoogde waardes aan bij suïcidale depressieve mensen:
According to new research, suicidal individuals have elevated levels of quinolinic acid in the fluid surrounding the central nervous system. The discovery could explain a missing link between inflammation and mental illness, said study researcher Lena Brundin, a professor of translational science and molecular medicine at Michigan State University. Previously, scientists had linked suicidal feelings to the kind of bodily inflammation that occurs during illness or stress, but they weren’t able to explain how inflammation could translate to depression, hopelessness and a desire to kill oneself.
The new study of 100 Swedish patients finds that the higher the level of quinolinic acid in the spinal fluid, the stronger their desire to commit suicide.
“The sicker the patient, the higher the quinolinic acid,” Brundin told LiveScience.
To find out, Brundin and her colleagues tested 100 Swedish adults for quinolinic acid, a compound known to be generated by inflammation and to have an effect in the brain due to its similarities to the neurotransmitter glutamate. This is a tough compound to test for, requiring not a simple blood draw but the extraction of cerebrospinal fluid, the clear, yellowish liquid that cushions the brain and spinal cord.
About two-thirds of the Swedish participants were tested right after hospitalization for a suicide attempt. The rest were healthy. The results revealed that the stronger the urge to commit suicide, the higher the levels of quinolinic acid in the spinal fluid.
Specifically, the neurotransmitter glutamate might offer new avenues for treatment. Glutamate is the neurotransmitter that quinolinic acid mimics. In a healthy brain, it plays an important role in exciting nerve cells. However, the discovery that quinolinic acid contributes to suicide or depression by playing copycat to glutamate suggests that targeting this neurotransmitter could provide relief.
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Quinolinic Acid: Suicide Attempts Linked To Chemical’s Presence In Spinal Fluid, Study SaysResearchers have found the first proof that a chemical in the brain called glutamate is linked to suicidal behavior, offering new hope for efforts to prevent people from taking their own lives.
Writing in the journal Neuropsychopharmacology, Michigan State University’s Lena Brundin and an international team of co-investigators present the first evidence that glutamate is more active in the brains of people who attempt suicide. Glutamate is an amino acid that sends signals between nerve cells and has long been a suspect in the search for chemical causes of depression.
“The findings are important because they show a mechanism of disease in patients,” said Brundin, associate professor of translational science and molecular medicine in MSU’s College of Human Medicine. “There’s been a lot of focus on another neurotransmitter called serotonin for about 40 years now. The conclusion from our paper is that we need to turn some of that focus to glutamate.”
Brundin and colleagues examined glutamate activity by measuring quinolinic acid – which flips a chemical switch that makes glutamate send more signals to nearby cells – in the spinal fluid of 100 patients in Sweden. About two-thirds of the participants were admitted to a hospital after attempting suicide and the rest were healthy.
They found that suicide attempters had more than twice as much quinolinic acid in their spinal fluid as the healthy people, which indicated increased glutamate signaling between nerve cells. Those who reported the strongest desire to kill themselves also had the highest levels of the acid.
The results also showed decreased quinolinic acid levels among a subset of patients who came back six months later, when their suicidal behavior had ended.
The findings explain why earlier research has pointed to inflammation in the brain as a risk factor for suicide. The body produces quinolinic acid as part of the immune response that creates inflammation.
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COUNTERING BRAIN CHEMICAL COULD PREVENT SUICIDESDus bij die Zweedse studie troffen ze bij suïcidale mensen verhoogde Quinolicic Acid waardes aan in het hersenruggenmergsvocht. Hoe hoger deze Quinolinc Acid des te erger de drang tot zelfmoord zo bleek. En deze waardes gingen omlaag zo'n 6 maanden later bij een deel van deze patiënten toen ook hun suïcidale gevoelens niet meer aanwezig waren.
Deze Quinolinic Acid bootst ook de functie van de meest voorkomende neurontransmitter
Glutamaat na en deze zijn beide betrokken bij overactivatie van de primaire glutamaat-receptor de
NMDA-Receptor.
Maar deze Quinolic Acid zorgt in hoge concentraties er ook voor dat de de zogenaamde
Glutamaat-Glutamine Cyclus wordt verstoord door de zogenaamde
Glutamine Synthetase enzyme te doen verhinderen. Hierdoor stijgt het glutamaat niveau soms zo hoog dat het neurologische schade veroorzaakt en ook nog eens voor een verdere aanmaak van die Quinolic Acid zorgt:
In normal cell conditions, astrocytes in the neuron will provide a glutamate-glutamine cycle, which results in reuptake of glutamate from the synapse into the pre-synaptic cell to be recycled, keeping glutamate from accumulating to lethal levels inside the synapse. At high concentrations, quinolinic acid inhibits glutamine synthetase, a critical enzyme in the glutamate-glutamine cycle. In addition, It can also promote glutamate release and block its reuptake by astrocytes. All three of these actions result in increased levels of glutamate activity that could be neurotoxic.[10]
This results in a loss of function of the cycle, and results in an accumulation of glutamate. This glutamate further stimulates the NMDA receptors, thus acting synergistically with quinolinic acid to increase its neurotoxic effect by increasing the levels of glutamate, as well as inhibiting its uptake. In this way, quinolinic acid self-potentiates its own toxicity.[10] Furthermore, quinolinic acid results in changes of the biochemistry and structure of the astrocytes themselves, resulting in an apoptotic response. A loss of astrocytes results in a pro-inflammatory effect, further increasing the initial inflammatory response which initiates quinolinic acid production
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Wikipedia
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