Editing Resveratrol

[[Information on nutritional supplements people with ALS have been taking]]

* [https://en.wikipedia.org/wiki/Resveratrol Wikipedia page]
* [http://www.medicalnewstoday.com/articles/241120.php Medical News Today]

== Effects on ALS ==

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}}

''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}}

''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}}

Resveratrol specifically '''inhibits the TRIF pathway in TLR3 and TLR4 signaling''', by targetting TBK1 and RIP1 in the TRIF complex. {{#pmid:16116226|youn2005}}

''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'''.''[5] 

''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.'' [6]

[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.

== Research article link collection ==

[http://alsanesthetics.org/research/solving-the-puzzle/potential-therapeutics-foci-of-intervention/117-resveratrol Research papers on resveratrol and ALS]

рохля электрическая 
<a href=https://samokhodnyye-elektricheskiye-telezhki.ru>https://samokhodnyye-elektricheskiye-telezhki.ru</a>

== References ==
  

[5]
<bibtex>
@article{Kutuk2006,
abstract = {In the present study we have studied the effect of resveratrol in signal transduction mechanisms leading to apoptosis in 3T3 fibroblasts when exposed to 4-hydroxynonenal (HNE). In order to gain insight into the mechanisms of apoptotic response by HNE, we followed MAP kinase and caspase activation pathways; HNE induced early activation of JNK and p38 proteins but downregulated the basal activity of ERK (1/2). We were also able to demonstrate HNE-induced release of cytochrome c from mitochondria, caspase-9, and caspase-3 activation. 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. Overexpression of dominant negative c-Jun and JNK1 in 3T3 fibroblasts prevented HNE-induced apoptosis, which indicates a role for JNK-c-Jun/AP-1 pathway. In light of the JNK-dependent induction of c-Jun/AP-1 activation and the protective role of resveratrol, these data may show a critical potential role for JNK in the cellular response against toxic products of lipid peroxidation. In this respect, resveratrol acting through MAP kinase pathways and specifically on JNK could have a role other than acting as an antioxidant-quenching reactive oxygen intermediate.},
author = {Kutuk, Ozgur and Poli, Giuseppe and Basaga, Huveyda},
doi = {10.1093/toxsci/kfj055},
issn = {1096-6080},
journal = {Toxicological sciences : an official journal of the Society of Toxicology},
keywords = {Aldehydes,Aldehydes: toxicity,Animals,Antioxidants,Antioxidants: pharmacology,Apoptosis,Apoptosis: drug effects,Caspase 3,Caspase 9,Caspases,Caspases: biosynthesis,Cytochromes c,Cytochromes c: metabolism,Dose-Response Relationship, Drug,Drug Antagonism,Fibroblasts,Fibroblasts: drug effects,Fibroblasts: metabolism,Fibroblasts: pathology,JNK Mitogen-Activated Protein Kinases,JNK Mitogen-Activated Protein Kinases: metabolism,MAP Kinase Kinase 4,MAP Kinase Kinase 4: metabolism,Mice,Mitochondria,Mitochondria: drug effects,Mitochondria: enzymology,Signal Transduction,Signal Transduction: drug effects,Stilbenes,Stilbenes: pharmacology,Swiss 3T3 Cells,Transcription Factor AP-1,Transcription Factor AP-1: metabolism},
mendeley-groups = {resveratrol},
month = mar,
number = {1},
pages = {120--32},
pmid = {16322078},
title = {{Resveratrol protects against 4-hydroxynonenal-induced apoptosis by blocking JNK and c-JUN/AP-1 signaling.}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/16322078},
volume = {90},
year = {2006}
}
</bibtex>

[6]
<bibtex>
@article{Baur2006,
abstract = {Resveratrol (3,5,4'-trihydroxystilbene) extends the lifespan of diverse species including Saccharomyces cerevisiae, Caenorhabditis elegans and Drosophila melanogaster. In these organisms, lifespan extension is dependent on Sir2, a conserved deacetylase proposed to underlie the beneficial effects of caloric restriction. Here we show that resveratrol shifts the physiology of middle-aged mice on a high-calorie diet towards that of mice on a standard diet and significantly increases their survival. 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 1$\alpha$ (PGC-1$\alpha$) 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. These data show that improving general health in mammals using small molecules is an attainable goal, and point to new approaches for treating obesity-related disorders and diseases of ageing.},
author = {Baur, J.A. and Pearson, K.J. and Price, N.L. and Jamieson, H.A. and Lerin, C. and Kalra, A. and Prabhu, V.V. and Allard, J.S. and Lopez-Lluch, G. and Lewis, K.},
issn = {0028-0836},
journal = {Nature},
keywords = {food intake,gene expression regulation,health status,high energy diet,longevity,metabolism,mice,mortality,oral administration,resveratrol},
language = {English},
mendeley-groups = {resveratrol},
title = {{Resveratrol improves health and survival of mice on a high-calorie diet}},
url = {http://agris.fao.org/agris-search/search.do?recordID=US201300758937},
year = {2006}
}
</bibtex>

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