voici un mix de mes "copier-coller" suite à mes recherches d'infos sur l'acide quinolinique et sujets associés. Je mets ça tel quel :
http://www.ncbi.nlm.nih.gov/pubmed/1531156 ---> lien entre lyme et acide quinolonique
neuroprotective kynurenic acid and the neurotoxic quinolinic acid
Kynurenic acid is an endogenous broad-spectrum antagonist of excitatory amino acid receptors
QUIN is a neurotoxic agent that generates free radicals, and in high concentration excites the NMDA receptors and causes excitotoxicity. It has similar neurotoxic effects to those of glutamate in the neocortex, striatum and hippocampus.
QUIN produces toxic free radicals
QUIN is able to induce several toxic effects, e.g. ATP exhaustion and oxidative neuronal cell death. Its role is cardinal for the modulation of critical cellular functions and the ion transport involved in excitotoxicity. QUIN can increase the generation of ROS (reactive oxygen species) and reactive nitrogen species by activating NMDA receptors, which increase the intracellular calcium level and result in the activation of xanthine oxidase
and nitric oxide (NO) synthase. At low arginine concentration, neuronal NO synthase generates NO and superoxide, favouring the production of the toxin peroxynitrite. Thus, the NMDA-induced excitotoxicity in neuronal cells is dependent on the arginine availability
An increasing concentration of QUIN leads to ROS formation in all brain regions
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ROS :
http://fr.wikipedia.org/wiki/D%C3%A9riv ... yg%C3%A8neLes dérivés réactifs de l'oxygène (DRO, en anglais reactive oxygen species, ROS) sont des espèces chimiques oxygénées telles que des radicaux libres, des ions oxygénés et des peroxydes, rendus chimiquement très réactifs par la présence d'électrons de valence non appariés.
Les DRO peuvent être d'origine exogène — produits par des rayonnements ionisants par exemple — ou bien endogène, apparaissant comme sous-produits du métabolisme normal de l'oxygène et jouant alors un rôle important dans la communication entre les cellules. Leur concentration peut cependant croître significativement en période de stress — sous l'effet de la chaleur ou de l'exposition aux ultraviolets par exemple — et endommager les structures cellulaires, ce qu'on appelle le stress oxydant.
Les cellules sont normalement capables de se défendre contre les dommages causés par les DRO à l'aide d'enzymes de type superoxyde dismutase, catalase, lactoperoxydase, glutathion peroxydase et peroxyrédoxine. De petites molécules antioxydantes telles que l'acide ascorbique (vitamine C), les tocophérols (vitamines E), l'acide urique et le glutathion jouent également un rôle très important comme antioxydants cellulaires. Les antioxydants polyphénoliques interviennent également dans l'élimination des radicaux libres. Le milieu extracellulaire semble en revanche moins armé contre les DRO, l'antioxydant plasmatique principal semblant être l'acide urique.
Les DRO sont des espèces chimiques à très forte réactivité capables d'oxyder les protéines, l'ADN et les membranes des cellules (attaque des lipides constitutifs par peroxydation lipidique): c'est une des théories actuelles du vieillissement (sénescence).
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ATP : L'ATP est l'abréviation de adénosine triphosphate, elle représente une molécule riche en énergie chimique, utilisée universellement par les cellules pour stocker l'énergie.
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Quinolinic acid is an excitotoxin in the CNS. It reaches pathological levels in response to inflammation in the brain
When inflammation occurs, quinolinic acid is produced in excessive levels through the kynurenine pathway. This leads to over excitation of the NMDA receptor, which results in an influx of Ca2+ into the neuron. High levels of Ca2+ in the neuron trigger an activation of destructive enzymatic pathways. These enzymes will degenerate crucial proteins in the cell and increase NO levels, leading to an apoptotic response by the cell, which results in cell death.
Quinolinic acid can also exert neurotoxicity through lipid peroxidation, as a result of its pro-oxidant properties.
researchers have demonstrated that increased quinolinic acid levels correlate with increased depressive symptoms
Increased levels of quinolinic acid might contribute to the apoptosis of astrocytes and certain neurons,
Quinolinic acid may contribute to the causes of amyotrophic lateral sclerosis (ALS). Researchers have found elevated levels of quinolinic acid in the cerebral spinal fluid (CSF), motor cortex, and spinal cord in ALS patients. These increased concentrations of quinolinic acid could lead to neurotoxicity. In addition, quinolinic acid is associated with overstimulating NMDA receptors on motor neurons.
Also, quinolinic acid plays a role in mitochondrial dysfunction in neurons.
Researchers have found a correlation between quinolinic acid and Alzheimer's disease.
Studies have found that there is a correlation between levels of quinolinic acid in cerebral spinal fluid (CSF) and HIV-associated neurocognitive disorder (HAND) severity. About 20% of HIV patients suffer from this disorder.
Quinolinic acid neurotoxicity is thought to play a role in Parkinson's disease.
In the initial stages of Huntington's disease, patients have substantially increased quinolinic acid levels, elevated quinolinic acid levels can lead to demyelination and cell death.
At least one study has suggested that quinolinic acid levels in neurological Lyme patients can be 40x higher than normal.
In Lyme it is the over production of quinolinic acid and the release of glutamate that overstimulates the NMDA receptor. The net result is that neurons rapidly and repeatedly fire and they become clogged with calcium, and become ineffective.
A neuron that is overstimulated past threshold repeatedly demyelinates, and can then interrupt other neurons in the neural complex. Without dendritic branching functioning properly we lose the ability to maintain complex neural networks.
So what can be done to minimize NMDA receptor overstimulation during antibiotic therapy or acute episodes of bacterial induced encephalopathy?
We know of two common OTC products that interfere with NMDA receptors. One is large doses of magnesium. Magnesium compete for the site causing agents like glutamate and quinolinic acid to be displaced. The effect is generally mild without side effects and may help Lyme patients remain more cognitive and alert.
(I took 600mg Calcium/300 mg Magnesium 3 times per day,)
If CoQ10 is deficient, nerve cells in the brain and elsewhere may not have the ability to withstand the overstimulation caused by excess glutamate.
As an anti-oxidant curcumin limits and decreases brain injury. Chronic Lyme infection increases a chemical in the brain called quinolinic acid. Quinolinic acid is elevated in numerous disorders like Alzheimer's Disease and Parkinson's. It is an agent that causes brain dysfunction and injury. Curcumin lowers quinolinic acid through its anti-oxidant effect. It also appears that curcumin raises a potent anti-oxidant called glutathione that is found in all of our cells. Glutathione prevents and repairs nerve injury. I recommend curcummin for anyone who has cognition problems with poor memory or difficulty processing information.
de beacam » Lun 11 Mar 2013 22:41 
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