Redox shift is due to Warburg effect and mitochondrial impairment.
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Toxicity of the spike protein of COVID-19 is a redox shift phenomenon: A novel therapeu... - 0 views
www.sciencedirect.com/...S0891584923005014
COVID19 COVID-19 cancer inflammation SARS-CoV-2 spike proteins COVID spikeopathy
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Long-term effects include redox shift and cellular anabolism as a result of the Warburg effect and mitochondrial dysfunction
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Lipoic acid and Methylene Blue have been shown to enhance the mitochondrial activity, relieve the Warburg effect and increase catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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Methylene Blue, Chlorine dioxide and Lipoic acid may help reduce long-term Covid-19 effects by stimulating the catabolism
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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direct consequence of redox iMeBalance, itself a consequence of decreased energy yield by the mitochondria
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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mitochondrial dysfunction and increased levels of lactate, which are important characteristics of metabolic shift and Warburg effect in many diseases
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cell division is the most sophisticated way to release entropy
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redox signaling plays an important role in regulating immune function and inflammation, and disruptions in this signaling can lead to excessive cytokine production and immune system activation
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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reduced extracellular environment in the elderly and the increased susceptibility to Covid-19 infection
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Redox signaling tightly modulates the inflammatory response and oxidative stress has been reported in acute Covid-19
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People at high risk are the elderly, patients suffering from metabolic syndrome such as obesity, or those suffering from chronic diseases such as cancer or inflammation
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COVID-19 patients with severe disease have higher levels of oxidative stress markers and lower antioxidant levels
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oxidative stress can activate the NLRP3 inflammasome, which is a protein complex that plays a key role in the cytokine storm
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inflammation leads to the formation of ROS and RNS, while redox iMeBalance results in cellular damage, which in turn triggers an inflammatory response
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persistently elevated mtROS triggers endothelial dysfunction and inflammation, which results in a vicious loop involving ROS, inflammation, and mitochondrial dysfunction
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IL-2 is highly up-regulated in Covid-19 patients [37], and IL-2 is known to significantly stimulate the generation of NO in patients
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Elevated levels of lactate, a characteristic of the Warburg effect, were also reported in the high-risk Covid-19
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vaccinated with RNA or DNA vaccines triggering the synthesis of the viral spike protein in human cells
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viral reactivation in varicella-zoster virus [55] or hepatitis [56], coagulopathy and resulting stroke and myocarditis following both DNA-based vaccines [57] and RNA-based vaccines
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characteristic of the Warburg effect is present in almost every disease and appears to be a central feature in most of the hallmarks of cancer
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inflammation, mitochondrial dysfunction and increased lactate concentrations in the extracellular fluid
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As the mitochondria are impaired, the infected cell cannot catabolize efficiently. It will release lactic acid in the blood stream
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Striking similarities are seen between cancer, Alzheimer's disease and Covid-19, all related to the Warburg effect
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Cancer, inflammation, Alzheimer's, and Parkinson's diseases share a common peculiarity, the inability of the cell to export entropy outside the body in the harmless form of heat
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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MEB relieves the Warburg effect [87], improves memory [77], is active in the treatment of depressive episodes [79,80] and reduces the importance of ischemic strokes
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It has been shown that Covid-19-patients treated with MEB, have a significant reduction in hospital stay duration and mortality
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MeB + can take a pair of electrons (of H atoms) and MeBH can release this pair easily, so that MeB is partially recycled like a catalyst
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MeB acts as an electron bridge between a donor (FADH2, FMNH, NADH) and an acceptor (complex IV of ETC or oxygen itself)
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As a coenzyme of pyruvate dehydrogenase (PDH), alpha-lipoic acid (ALA) initiates the formation of acetyl-CoA to feed the TCA cycle
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ALA enhances the catabolism of carbon. cycle and therefore may reduce the Warburg effect and consequently, lactate production
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Methylene Blue plays a similar role after the TCA cycle, by carrying electrons to complex IV of the electron transport chain
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Drugs such as lipoic acid and MeB, which target the metabolism, decrease the redox shift by increasing catabolism
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Lower low density lipid cholesterol levels are associated with Parkinson's disease - 0 views
www.ncbi.nlm.nih.gov/...PMC1906875
LDL cholesterol Parkinson's Parkinson's disease statins Parkinsons disease brain health low density cholesterol
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shared by Nathan Goodyear on 20 Feb 16
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Stuck at the bench: Potential natural neuroprotective compounds for concussion - 0 views
www.ncbi.nlm.nih.gov/...PMC3205506
concussions concussion natural therapies brain curcumin omega 3 resveratrol green tea EGCG EPA DHA vitamin E vitamin c vitamin D
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Long-chain polyunsaturated fatty acids, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are highly enriched in neuronal synaptosomal plasma membranes and vesicles
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effective supplementation and/or increased ingestion of dietary sources rich in EPA and DHA, such as cold-water fish species and fish oil, may help improve a multitude of neuronal functions, including long-term potentiation and cognition.
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multiple preclinical studies have suggested that DHA and/or EPA supplementation may have potential benefit through a multitude of diverse, but complementary mechanisms
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pre-injury dietary supplementation with fish oil effectively reduces post-traumatic elevations in protein oxidation
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The benefits of pre-traumatic DHA supplementation have not only been independently confirmed,[150] but DHA supplementation has been shown to significantly reduce the number of swollen, disconnected and injured axons when administered following traumatic brain injury.
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DHA has provided neuroprotection in experimental models of both focal and diffuse traumatic brain injury
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potential mechanisms of neuroprotection, in addition to DHA and EPA's well-established anti-oxidant and anti-inflammatory properties
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Despite abundant laboratory evidence supporting its neuroprotective effects in experimental models, the role of dietary DHA and/or EPA supplementation in human neurological diseases remains uncertain
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Several population-based, observational studies have suggested that increased dietary fish and/or omega-3 polyunsaturated fatty acid consumption may reduce risk for ischemic stroke in several populations
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Randomized control trials have also demonstrated significant reductions in ischemic stroke recurrence,[217] relative risk for ischemic stroke,[2] and reduced incidence of both symptomatic vasospasm and mortality following subarachnoid hemorrhage
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curcumin has gained much attention from Western researchers for its potential therapeutic benefits in large part due to its potent anti-oxidant[128,194,236] and anti-inflammatory properties
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Curcumin is highly lipophilic and crosses the blood-brain barrier enabling it to exert a multitude of different established neuroprotective effects
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in the context of TBI, a series of preclinical studies have suggested that pre-traumatic and post-traumatic curcumin supplementation may bolster the brain's resilience to injury and serve as a valuable therapeutic option
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Curcumin may confer significant neuroprotection because of its ability to act on multiple deleterious post-traumatic, molecular cascades
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studies demonstrated that both pre- and post-traumatic curcumin administration resulted in a significant reduction of neuroinflammation via inhibition of the pro-inflammatory molecules interleukin 1β and nuclear factor kappa B (NFκB)
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no human studies have been conducted with respect to the effects of curcumin administration on the treatment of TBI, subarachnoid or intracranial hemorrhage, epilepsy or stroke
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studies have demonstrated that resveratrol treatment reduces brain edema and lesion volume, as well as improves neurobehavioral functional performance following TBI
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green tea consumption or supplementation with its derivatives may bolster cognitive function acutely and may slow cognitive decline
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At least one population based study, though, did demonstrate that increased green tea consumption was associated with a reduced risk for Parkinson's disease independent of total caffeine intake
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a randomized, placebo-controlled trial demonstrated that administration of green tea extract and L-theanine, over 16 weeks of treatment, improved indices of memory and brain theta wave activity on electroencephalography, suggesting greater cognitive alertness
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Other animal studies have also demonstrated that theanine, another important component of green tea extract, exerts a multitude of neuroprotective benefits in experimental models of ischemic stroke,[63,97] Alzheimer's disease,[109] and Parkinson's disease
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Theanine, like EGCG, contains multiple mechanisms of neuroprotective action including protection from excitotoxic injury[97] and inhibition of inflammation
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More recent research has suggested that vitamin D supplementation and the prevention of vitamin D deficiency may serve valuable roles in the treatment of TBI and may represents an important and necessary neuroprotective adjuvant for post-TBI progesterone therapy
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Progesterone is one of the few agents to demonstrate significant reductions in mortality following TBI in human patients in preliminary trials
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in vitro and in vivo studies have suggested that vitamin D supplementation with progesterone administration may significantly enhance neuroprotection
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Vitamin D deficiency may increase inflammatory damage and behavioral impairment following experimental injury and attenuate the protective effects of post-traumatic progesterone treatment.[37]
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emerging evidence has suggested that daily intravenous administration of vitamin E following TBI significantly decreases mortality and improves patient outcomes
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high dose vitamin C administration following injury stabilized or reduced peri-lesional edema and infarction in the majority of patients receiving post-injury treatment
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it has been speculated that combined vitamin C and E therapy may potentiate CNS anti-oxidation and act synergistically with regards to neuroprotection
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one prospective human study has found that combined intake of vitamin C and E displays significant treatment interaction and reduces the risk of stroke
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Pycnogenol has demonstrated the ability to slow or reduce the pathological processes associated with Alzheimer's disease
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Pcynogenol administration, in a clinical study of elderly patients, led to improved cognition and reductions in markers of lipid peroxidase
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One other point of consideration is that in neurodegenerative disease states like Alzheimer's disease and Parkinson's disease, where there are high levels of reactive oxygen species generation, vitamin E can tend to become oxidized itself. For maximal effectiveness and to maintain its anti-oxidant capacity, vitamin E must be given in conjunction with other anti-oxidants like vitamin C or flavonoids
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These various factors might account for the null effects of alpha-tocopherol supplementation in patients with MCI and Alzheimer's disease
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preliminary results obtained in a pediatric population have suggested that post-traumatic oral creatine administration (0.4 g/kg) given within four hours of traumatic brain injury and then daily thereafter, may improve both acute and long-term outcomes
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Acutely, post-traumatic creatine administration seemed to reduce duration of post-traumatic amnesia, length of time spent in the intensive care unit, and duration of intubation
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At three and six months post-injury, subjects in the creatine treatment group demonstrated improvement on indices of self care, communication abilities, locomotion, sociability, personality or behavior and cognitive function when compared to untreated controls
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patients in the creatine-treatment group were less likely to experience headaches, dizziness and fatigue over six months of follow-up
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CNS creatine is derived from both its local biosynthesis from the essential amino acids methionine, glycine and arginine
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Studies of patients with CNS creatine deficiency and/or murine models with genetic ablation of creatine kinase have consistently demonstrated significant neurological impairment in the absence of proper creatine, phosphocreatine, or creatine kinase function; thus highlighting its functional importance
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chronic dosing may partially reverse neurological impairments in human CNS creatine deficiency syndromes
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Several studies have suggested that creatine supplementation may also reduce oxidative DNA damage and brain glutamate levels in Huntington disease patients
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Another study highlighted that creatine supplementation marginally improved indices of mood and reduced the need for increased dopaminergic therapy in patients with Parkinson's disease
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VITAMINS AND ENTACAPONE IN LEVODOPA-INDUCED HYPERHOMOCYSTEINEMIA: A RANDOMIZED CONTROLL... - 0 views
www.neurology.org/...1440.extract
Levodopa parkinson's disease Parkinson's homocysteine neurodegenerative disease vitamins
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Study Suggests Coenzyme Q10 Slows Functional Decline in Parkinson's Disease: National I... - 0 views
www.ninds.nih.gov/...kinsons_coenzymeq10_101402.htm
CoQ10 Parkinson's disease Huntington's ecitotoxic neurotoxic
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Randomized, double-blind, pilot evaluation of int... [Mov Disord. 2009] - PubMed - NCBI - 0 views
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Advanced Glycation End Products in Alzheimer's Disease and Other Neurodegenerative Dise... - 0 views
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The evidence basis for coenzyme Q therapy in oxida... [Mitochondrion. 2007] - PubMed re... - 0 views
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In some mitochondrial diseases and other commoner disorders such as cardiac disease and Parkinson's disease low mitochondrial or tissue levels of CoQ10 have been demonstrated providing an obvious rationale for supplementation
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Mitochondrial dysfunction in Parkinson's disease. [Biochim Biophys Acta. 2010] - PubMed... - 0 views
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any lines of evidence suggest that mitochondrial dysfunction plays a central role in the pathogenesis of Parkinson's disease (PD)
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The emerging role of nutrition in Parkinson's disease - 0 views
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Good review of the current data on the role of nutrition in Parkinson's disease. Take home, a lot of data is conflicting. But the figure at the end does well to summarize: diet rich in polyphenols in fruits/veggies, carotenoids, resveratrol, Vitamin C, D, E, and MUFA and PUFA are neuroprotective compared to dairy being neurodegenerative.
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Erectile Function and Risk of Parkinson's Disease - 0 views
aje.oxfordjournals.org/...1446.short
ED erectile dysfunction Parkinson's parkinson's disease inflammation
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Annals of Internal Medicine | Gene-Diet Interactions in Brain Aging and Neurodegenerati... - 0 views
annals.org/article.aspx
diet calorie neurodegenerative disease brain neurology parkinson's disease Alzheimer's disease aging
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it appears that dietary restriction promotes neuronal survival, plasticity, and even neurogenesis by inducing a mild cellular stress response that involves activation of genes that encode proteins designed to promote neuronal growth and surviva
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Studies of animal models of Alzheimer disease and Parkinson disease have shown that, by decreasing homocysteine levels, dietary folic acid can be neuroprotective
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The current average daily calorie intake of Americans is approximately 2700 for women and more than 3000 for men
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Neuroinflammation in Parkinson's disease: a ta... [Lancet Neurol. 2009] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...19296921
glial cells Parkinson's disease neurodegenerative disorders inflammation neuroinflammation
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Mitochondrial pathobiology in Parkinson's disease ... [J Alzheimers Dis. 2010] - PubMed... - 0 views
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ScienceDirect.com - Journal of Clinical Neuroscience - Testosterone improves motor func... - 0 views
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Exposure to pesticides or solvents and risk of Parkinson disease - 0 views
www.neurology.org/...2035.abstract
pesticides disease Parkinson's Parkinson's disease solvents environmental toxins toxins paraquat
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Exposure to pesticides or solvents and risk of Parkinson disease - 0 views
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Glutathione and Parkinson's Disease - ACAM Integrative Medicine (IM) Blog - 0 views
acam.typepad.com/...ne-and-parkinsons-disease.html
IV glutathione Parkinson's disease treatment therapy
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Coenzyme Q10 in neurodegenerative diseases. [Curr Med Chem. 2003] - PubMed result - 0 views
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supplemental coenzyme Q(10) can slow the functional decline in these disorders, particularly Parkinson's disease.