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[[Information on nutritional supplements people with ALS have been taking]]
 
[[Information on nutritional supplements people with ALS have been taking]]
  
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* [https://en.wikipedia.org/wiki/Resveratrol Wikipedia page]
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[https://en.wikipedia.org/wiki/Resveratrol Wikipedia page]
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* [http://www.medicalnewstoday.com/articles/241120.php Medical News Today]
 
  
 
== Effects on ALS ==
 
== Effects on ALS ==
  
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In rat brain cortical motoneuron primary culture, resveratrol '''protects against neurotoxic effects and antagonizes the [Ca(+2)](c) elevation''' produced by ALS/CSF. However, riluzole does not afford protection and antagonizes the resveratrol-elicited neuroprotective effects. {{#pmid:21983205|yanez2011}}
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In rat brain cortical motoneuron primary culture, resveratrol protects against neurotoxic effects and antagonizes the [Ca(+2)](c) elevation produced by ALS/CSF. However, riluzole does not afford protection and antagonizes the resveratrol-elicited neuroprotective effects. [1]
  
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''Our results indicate that resveratrol potently '''reduced LPS-induced PGE2 synthesis and the formation of 8-iso-PGF2 alpha, a measure of free radical production'''. Interestingly, resveratrol dose-dependently '''reduced the expression (mRNA and protein) of mPGES-1, which is a key enzyme responsible for the synthesis of PGE2 by activated microglia''', whereas resveratrol did not affect the expression of COX-2. Resveratrol is therefore the '''first known inhibitor which specifically prevents mPGES-1 expression without affecting COX-2 levels'''. Another important observation of the present study is that other COX-1 selective inhibitors (SC-560 and Valeroyl Salicylate) potently reduced PGE2 and 8-iso-PGF2 alpha production by LPS-activated microglia. These findings suggest that the naturally occurring polyphenol resveratrol is '''able to reduce microglial activation''', an effect that might help to explain its neuroprotective effects in several in vivo models of brain injury.'' {{#pmid:17927823|candelario2007}}
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Our results indicate that resveratrol potently reduced LPS-induced PGE2 synthesis and the formation of 8-iso-PGF2 alpha, a measure of free radical production.  
  
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''Here, we report that a human homologue of SIR2, SIRT1, is upregulated in mouse models for AD, ALS and in primary neurons challenged with neurotoxic insults. '''In cell-based models for AD/tauopathies and ALS, SIRT1 and resveratrol, a SIRT1-activating molecule, both promote neuronal survival'''. In the inducible p25 transgenic mouse, a model of AD and tauopathies, resveratrol reduced neurodegeneration in the hippocampus, prevented learning impairment, and decreased the acetylation of the known SIRT1 substrates PGC-1alpha and p53.'' {{#pmid:17581637|kim2007}}
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''Interestingly, resveratrol dose-dependently reduced the expression (mRNA and protein) of mPGES-1, which is a key enzyme responsible for the synthesis of PGE2 by activated microglia, whereas resveratrol did not affect the expression of COX-2. Resveratrol is therefore the first known inhibitor which specifically prevents mPGES-1 expression without affecting COX-2 levels. Another important observation of the present study is that other COX-1 selective inhibitors (SC-560 and Valeroyl Salicylate) potently reduced PGE2 and 8-iso-PGF2 alpha production by LPS-activated microglia. These findings suggest that the naturally occurring polyphenol resveratrol is able to reduce microglial activation, an effect that might help to explain its neuroprotective effects in several in vivo models of brain injury.'' [2]
  
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Resveratrol specifically '''inhibits the TRIF pathway in TLR3 and TLR4 signaling''', by targetting TBK1 and RIP1 in the TRIF complex. {{#pmid:16116226|youn2005}}
 
  
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''Resveratrol effectively '''prevented HNE-induced JNK and caspase activation, and hence apoptosis'''. Activation of AP-1 along with increased c-Jun and phospho-c-Jun levels could be inhibited by pretreatment of cells with resveratrol. Moreover, '''Nrf2 downregulation by HNE could also be blocked by resveratrol'''.''{{#pmid:16322078|kutuk2006}}
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== References ==
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''Resveratrol produces changes associated with longer lifespan, including '''increased insulin sensitivity, reduced insulin-like growth factor-1 (IGF-I) levels, increased AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) activity, increased mitochondrial number, and improved motor function'''. Parametric analysis of gene set enrichment revealed that resveratrol opposed the effects of the high-calorie diet in 144 out of 153 significantly altered pathways.'' {{#pmid:17086191|baur2006}}
 
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[http://www.resveratrolnews.com/how-modern-medicine-obfuscates-resveratrol-science/833/ Resveratrol News]: Collection of sources suggesting that low dosing (up to about 150 mg/day) is beneficial but high doses harmful.
 
  
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== Research article link collection ==
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[1]
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<bibtex>
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@article{Yanez2011,
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abstract = {The neurotoxic effects of cerebrospinal fluid (CSF) from patients suffering amyotrophic lateral sclerosis (ALS), have been reported by various authors. However, variable results have been communicated and the mechanism of such neurotoxicity has been attributed to excess glutamate concentrations in ALS/CSF. We have studied here the properties of 14 CSFs from control patients and 29 CSFs from patients of ALS. We found that while ALS/CSF impairs the viability of rat brain cortical motoneurons maintained in primary cultures, this effect seemed to be exerted through a glutamate-independent mechanism. Resveratrol protected against such neurotoxic effects and antagonized the [Ca(+2)](c) elevation produced by ALS/CSF. However, riluzole did not afford protection and antagonized the resveratrol-elicited neuroprotective effects. We conclude that ALS/CSF elicited neurotoxicity on in vitro cultures of rat brain cortical motor neurons may become a sound microassay to test available novel multitargeted neuroprotective compounds with potential therapeutic application in ALS patients.},
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author = {Y\'{a}\~{n}ez, Matilde and Gal\'{a}n, Luc\'{\i}a and Mat\'{\i}as-Guiu, Jorge and Vela, Alvaro and Guerrero, Antonio and Garc\'{\i}a, Antonio G},
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doi = {10.1016/j.brainres.2011.09.025},
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issn = {1872-6240},
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journal = {Brain research},
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keywords = {Adult,Aged,Amyotrophic Lateral Sclerosis,Amyotrophic Lateral Sclerosis: cerebrospinal fluid,Animals,Calcium,Calcium: metabolism,Cell Death,Cell Death: drug effects,Cells, Cultured,Cerebral Cortex,Cerebral Cortex: cytology,Dose-Response Relationship, Drug,Double-Blind Method,Drug Interactions,Embryo, Mammalian,Female,Glutamic Acid,Glutamic Acid: pharmacology,Humans,L-Lactate Dehydrogenase,L-Lactate Dehydrogenase: metabolism,Male,Middle Aged,Motor Neurons,Motor Neurons: drug effects,Neuroprotective Agents,Neuroprotective Agents: pharmacology,Pregnancy,Rats,Riluzole,Riluzole: pharmacology,Stilbenes,Stilbenes: pharmacology},
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mendeley-groups = {resveratrol},
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month = nov,
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pages = {77--86},
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pmid = {21983205},
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title = {{CSF from amyotrophic lateral sclerosis patients produces glutamate independent death of rat motor brain cortical neurons: protection by resveratrol but not riluzole.}},
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url = {http://www.ncbi.nlm.nih.gov/pubmed/21983205},
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volume = {1423},
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year = {2011}
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}
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</bibtex>
  
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[http://alsanesthetics.org/research/solving-the-puzzle/potential-therapeutics-foci-of-intervention/117-resveratrol Research papers on resveratrol and ALS]
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[2]
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<bibtex>
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@article{Candelario-Jalil2007,
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abstract = {BACKGROUND: Neuroinflammatory responses are triggered by diverse ethiologies and can provide either beneficial or harmful results. Microglial cells are the major cell type involved in neuroinflammation, releasing several mediators, which contribute to the neuronal demise in several diseases including cerebral ischemia and neurodegenerative disorders. Attenuation of microglial activation has been shown to confer protection against different types of brain injury. Recent evidence suggests that resveratrol has anti-inflammatory and potent antioxidant properties. It has been also shown that resveratrol is a potent inhibitor of cyclooxygenase (COX)-1 activity. Previous findings have demonstrated that this compound is able to reduce neuronal injury in different models, both in vitro and in vivo. The aim of this study was to examine whether resveratrol is able to reduce prostaglandin E2 (PGE2) and 8-iso-prostaglandin F2alpha (8-iso-PGF2 alpha) production by lipopolysaccharide (LPS)-activated primary rat microglia.
  
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рохля электрическая
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METHODS: Primary microglial cell cultures were prepared from cerebral cortices of neonatal rats. Microglial cells were stimulated with 10 ng/ml of LPS in the presence or absence of different concentrations of resveratrol (1-50 microM). After 24 h incubation, culture media were collected to measure the production of PGE2 and 8-iso-PGF2 alpha using enzyme immunoassays. Protein levels of COX-1, COX-2 and microsomal prostaglandin E synthase-1 (mPGES-1) were studied by Western blotting after 24 h of incubation with LPS. Expression of mPGES-1 at the mRNA level was investigated using reverse transcription-polymerase chain reaction (RT-PCR) analysis.
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<a href=https://samokhodnyye-elektricheskiye-telezhki.ru>https://samokhodnyye-elektricheskiye-telezhki.ru</a>
 
  
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== References ==
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RESULTS: Our results indicate that resveratrol potently reduced LPS-induced PGE2 synthesis and the formation of 8-iso-PGF2 alpha, a measure of free radical production. Interestingly, resveratrol dose-dependently reduced the expression (mRNA and protein) of mPGES-1, which is a key enzyme responsible for the synthesis of PGE2 by activated microglia, whereas resveratrol did not affect the expression of COX-2. Resveratrol is therefore the first known inhibitor which specifically prevents mPGES-1 expression without affecting COX-2 levels. Another important observation of the present study is that other COX-1 selective inhibitors (SC-560 and Valeroyl Salicylate) potently reduced PGE2 and 8-iso-PGF2 alpha production by LPS-activated microglia.
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[[Category:Supplement data pages]]
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CONCLUSION: These findings suggest that the naturally occurring polyphenol resveratrol is able to reduce microglial activation, an effect that might help to explain its neuroprotective effects in several in vivo models of brain injury.},
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author = {Candelario-Jalil, Eduardo and de Oliveira, Antonio C Pinheiro and Gr\"{a}f, Sybille and Bhatia, Harsharan S and H\"{u}ll, Michael and Mu\~{n}oz, Eduardo and Fiebich, Bernd L},
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doi = {10.1186/1742-2094-4-25},
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issn = {1742-2094},
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journal = {Journal of neuroinflammation},
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keywords = {Animals,Animals, Newborn,Antioxidants,Antioxidants: pharmacology,Cells, Cultured,Cyclooxygenase 1,Cyclooxygenase 1: drug effects,Cyclooxygenase 1: metabolism,Cyclooxygenase Inhibitors,Cyclooxygenase Inhibitors: pharmacology,Dinoprost,Dinoprost: analogs \& derivatives,Dinoprost: antagonists \& inhibitors,Dinoprost: biosynthesis,Dinoprostone,Dinoprostone: antagonists \& inhibitors,Dinoprostone: biosynthesis,Down-Regulation,Down-Regulation: drug effects,Down-Regulation: physiology,Encephalitis,Encephalitis: drug therapy,Encephalitis: metabolism,Encephalitis: physiopathology,Free Radical Scavengers,Free Radical Scavengers: pharmacology,Free Radicals,Free Radicals: antagonists \& inhibitors,Free Radicals: metabolism,Gliosis,Gliosis: drug therapy,Gliosis: metabolism,Gliosis: physiopathology,Inflammation Mediators,Inflammation Mediators: pharmacology,Lipopolysaccharides,Lipopolysaccharides: pharmacology,Microglia,Microglia: drug effects,Microglia: metabolism,Oxidative Stress,Oxidative Stress: drug effects,Oxidative Stress: physiology,Rats,Stilbenes,Stilbenes: pharmacology},
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mendeley-groups = {resveratrol},
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month = jan,
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pages = {25},
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pmid = {17927823},
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title = {{Resveratrol potently reduces prostaglandin E2 production and free radical formation in lipopolysaccharide-activated primary rat microglia.}},
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url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2100038\&tool=pmcentrez\&rendertype=abstract},
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volume = {4},
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year = {2007}
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}
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</bibtex>

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