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Post by Admin on May 16, 2011 18:45:50 GMT -5
The article discusses the relationship between inflammation and depression. Although the article discusses cytokines and glutamate, its worth noting that inflammatory agents, and Omega 3 anti inflammatory, can in some cases become pro-inflammatory by a process of oxidization leading to free radicals = inflammation. It depends on the individual's biochemistry. It may help some, whilst causing more damage to others. The mediators for inflammation differs from the discussion below, nevertheless worth considering. A few lines from the article - note the connection with NMDA recptors agonist, glutamate, quinolinic acid. Inflammation, Glutamate, and Glia in Depression: A Literature ReviewInflammatory mediators can, through activation of the kynurenine pathway (Figure 1), increase glutamate receptor agonism. The two main end-products of the kynurenine pathway bind to NMDA receptors: Kynurenic acid is an NMDA receptor antagonist, while quinolinic acid is an NMDA receptor agonist. Although IDO, the rate-limiting enzyme in the kynurenine pathway, is expressed in multiple cell types, microglia are the only cells in the central nervous system that express the complete enzymatic pathway required for the synthesis of quinolinic acid.55 Therefore, inflammatory mediators acting on microglia will increase the quinolinic acid to kynurenic acid ratio, leading to net NMDA agonism.15,56 In addition to NMDA agonist action, quinolinic acid directly causes release of glutamate.57 Thus, inflammatory mediators can cause an environment of excess glutamate receptor agonism and resultant neurotoxicity. Although glutamate can cause neurotoxicity, it is important to point out that neurotoxicity in depression has not been unequivocally demonstrated. www.cnsspectrums.com/aspx/articledetail.aspx?articleid=1590
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Post by Admin on May 16, 2011 19:05:42 GMT -5
Another article which explains clearly in simple lingo, about the relationship between long term chronic stress, cytokines and the new discovery of an immune cell which is produced in the bone marrow, circulates and goes to the brain. It links with cytokines, NTF and glucosteroids, in this case, instead of being anti-inflammatory and protects against infections, leads to more stress, inflammation and anxiety. It all ties in with the fact, that there are options worth looking at, dietary modification, Yoga, Tai Chi, Qi Gong, and specific breathing methods, which are known to increase DHEA, endorphins, serotonin and other health benefits. Article: Researchers See a 'Picture' of Threat in the Brain: Work May Lead to New Model of NeuroinflammationScienceDaily (May 9, 2011) — A team of researchers is beginning to see exactly what the response to threats looks like in the brain at the cellular and molecular levels. The response to social stress also caused an increase in the amounts of some inflammatory cytokines in the brain, including interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-a) which are linked to inflammation. These cytokine responses correlated with an insensitivity of MPCs to glucocorticoids, hormones that normally inhibit inflammation in the body. So the research team saw these and other cellular changes occurring in the brain following the stress, at the same time they were seeing the behavioral changes -- the anxiety-like behavior. www.sciencedaily.com/releases/2011/05/110503133058.htm"We found that in the stressed animals, a certain type of immune cell (myeloid progenitor cell, or MPC), produced in the bone marrow, entered the circulatory system and migrated to the brain," explained Godbout.
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Post by beebs on Aug 6, 2011 7:40:10 GMT -5
The article below discusses Grape Seed extract. I use to take this years ago, before the ADRs. Some floxies and others suffering brain fog and other neuro symptoms reported improvement taking Grape Seeds Extracts. Grape seed proanthocyanidin extract inhibits glutamate-induced cell death through inhibition of calcium signals and nitric oxide formation in cultured rat hippocampal neuronsSeo Hee Ahn email, Hee Jung Kim email, Imju Jeong email, Yi Jae Hong email, Myung Jun Kim email, Duck Joo Rhie email, Yang Hyeok Jo email, Sang June Hahn email and Shin Hee Yoon email BMC Neuroscience 2011, 12:78doi:10.1186/1471-2202-12-78 Published: 3 August 2011 Abstract (provisional) Background Proanthocyanidin is a polyphenolic bioflavonoid with known antioxidant activity. Some flavonoids have a modulatory effect on [Ca2+]i. Although proanthocyanidin extract from blueberries reportedly affects Ca2+ buffering capacity, there are no reports on the effects of proanthocyanidin on glutamate-induced [Ca2+]i or cell death. In the present study, the effects of grape seed proanthocyanidin extract (GSPE) on glutamate-induced excitotoxicity was investigated through calcium signals and nitric oxide (NO) in cultured rat hippocampal neurons. Results Pretreatment with GSPE (0.3-10 mug/ml) for 5 min inhibited the [Ca2+]i increase normally induced by treatment with glutamate (100 muM) for 1 min, in a concentration-dependent manner. Pretreatment with GSPE (6 mug/ml) for 5 min significantly decreased the [Ca2+]i increase normally induced by two ionotropic glutamate receptor agonists, N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA). GSPE further decreased AMPA-induced response in the presence of 1 muM nimodipine. However, GSPE did not affect the 50 mM K+-induced increase in [Ca2+]i. GSPE significantly decreased the metabotropic glutamate receptor agonist (RS)-3,5-Dihydroxyphenylglycine-induced increase in [Ca2+]i, but it did not affect caffeine-induced response. GSPE (0.3-6 mug/ml) significantly inhibited synaptically induced [Ca2+]i spikes by 0.1 mM [Mg2+]o. In addition, pretreatment with GSPE (6 mug/ml) for 5 min inhibited 0.1 mM [Mg2+]o- and glutamate-induced formation of NO. Treatment with GSPE (6 mug/ml) significantly inhibited 0.1 mM [Mg2+]o- and oxygen glucose deprivation-induced neuronal cell death. Conclusions All these data suggest that GSPE inhibits 0.1 mM [Mg2+]o- and oxygen glucose deprivation-induced neurotoxicity through inhibition of calcium signals and NO formation in cultured rat hippocampal neurons. www.biomedcentral.com/1471-2202/12/78/abstract
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Post by beebs on Dec 19, 2012 16:20:59 GMT -5
Full article access: www.lef.org/magazine/mag2011/ss2011_Neutralize-a-Lethal-Enzyme_01.htmBeware if you have problems with certains foods, & issues with TPRV and vanilloid receptors etc.. May excerbate symptoms. Neuroprotection and Brain HealthConstituents of a resin from a boswellia species have been shown to be potent stimulators of a brain receptor system called TRPV3 that lowers anxiety and exerts antidepressant-like effects.61 Neuroprotection and Brain Health A major component of Boswellia carterri (called Incensole acetate) inhibits inflammatory mediators in brain tissue, an effect that offers significant hope in treatment of brain injury.62 That's because a dangerous inflammatory response follows brain injury within hours, contributing to a substantial portion of the long-lasting neurological deficit. Incensole acetate specifically inhibits degeneration of brain cells in the hippocampus, the region responsible for memory processing.62 Animal models confirm this effect. Laboratory rats treated with a drug to impair memory, along with boswellia extract, performed significantly better on tests involving spatial orientation and learning than did animals treated with the drug alone.63 A similar result was shown in healthy animals not treated with a memory-destroying drug. Extracts of Boswellia papyrifera—one of five species of boswellia used in the making of frankincense— increase spatial memory retention, enabling the animals to quickly find their way out of a maze.64
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Post by beebs on Jan 27, 2013 18:03:52 GMT -5
Excerpt from an article showing the importance of gut flora and neurotransmitters. I would choose diet over probiotics to enhance the immune system and gut microbia. "Lactobacillus reuteri, a potential probiotic known to modulate the immune system26 decreases anxiety as measured on the elevated plus maze as well as reducing the stress-induced increase of corticosterone in mice.27 This probiotic alters the mRNA expression of both GABAA and GABAB receptors in the central nervous system. Alterations in these receptors are associated with anxious and depressive-like behaviors in animal models. Vagotomy in these animals prevented the anxiolytic and antidepressant effects of this bacterium as well as the effects on the central GABA receptors. This suggests that parasympathetic innervation is necessary for L. reuteri to participate in the microbiota-brain interaction. Previous studies28 have shown that probiotic agents can modulate antidepressant-like behavior with Bifidobacterium infantis having antidepressant properties in the forced swim test, a well-established model in the evaluation of pharmacological antidepressant activity.29 Chronic B. infantis administration also led to a suppression in stimulation-induced increases in peripheral pro-inflammatory cytokines and increases in plasma tryptophan,28 both of which have been implicated in depression.30,31 We have also investigated the impact of B. infantis on a preclinical model of IBS (maternal separation model)32 and showed that this bacterium was able to reverse some of the early-life stress-induced changes. Taken together, it is clear that certain probiotic strains can modulate various aspects of the microbiome-gut-brain axis.33 However, these effects are bacterial strain dependent and care must be taken in extrapolating data obtained from one organism to another. Nonetheless, the accumulating data suggest a clear ability of probiotic and potential probiotic strains to modulate brain and behavior." Full article: onlinelibrary.wiley.com/doi/10.1111/j.1365-2982.2010.01664.x/full
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