Editing Curcumin

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

[https://en.wikipedia.org/wiki/Curcumin Wikipedia page]


== Effect of curcumin on ALS ==

Curcumin is an antioxidant and a strong inducer of heat shock response. [1] It attenuates glutamate-induced HT22 cell death by suppressing MAP kinase signaling. [2]

== Discussion threads on the ALSTDI forum ==

[http://www.alstdi.org/forum/yaf_postst44482_curcumin.aspx Curcumin]


== Regulated pathways ==

Inactivates JNK and p38 [2].

== Where to get it ==



== References ==

[1]
<bibtex>
@article{Calabrese2006,
abstract = {Reduced expression and/or activity of antioxidant proteins lead to oxidative stress, accelerated aging and neurodegeneration. However, while excess reactive oxygen species (ROS) are toxic, regulated ROS play an important role in cell signaling. Perturbation of redox status, mutations favoring protein misfolding, altered glyc(osyl)ation, overloading of the product of polyunsaturated fatty acid peroxidation (hydroxynonenals, HNE) or cholesterol oxidation, can disrupt redox homeostasis. Collectively or individually these effects may impose stress and lead to accumulation of unfolded or misfolded proteins in brain cells. Alzheimer's (AD), Parkinson's and Huntington's disease, amyotrophic lateral sclerosis and Friedreich's ataxia are major neurological disorders associated with production of abnormally aggregated proteins and, as such, belong to the so-called "protein conformational diseases". The pathogenic aggregation of proteins in non-native conformation is generally associated with metabolic derangements and excessive production of ROS. The "unfolded protein response" has evolved to prevent accumulation of unfolded or misfolded proteins. Recent discoveries of the mechanisms of cellular stress signaling have led to new insights into the diverse processes that are regulated by cellular stress responses. The brain detects and overcomes oxidative stress by a complex network of "longevity assurance processes" integrated to the expression of genes termed vitagenes. Heat-shock proteins are highly conserved and facilitate correct protein folding. Heme oxygenase-1, an inducible and redox-regulated enzyme, has having an important role in cellular antioxidant defense. An emerging concept is neuroprotection afforded by heme oxygenase by its heme degrading activity and tissue-specific antioxidant effects, due to its products carbon monoxide and biliverdin, which is then reduced by biliverdin reductase in bilirubin. There is increasing interest in dietary compounds that can inhibit, retard or reverse the steps leading to neurodegeneration in AD. Specifically any dietary components that inhibit inappropriate inflammation, AbetaP oligomerization and consequent increased apoptosis are of particular interest, with respect to a chronic inflammatory response, brain injury and beta-amyloid associated pathology. Curcumin and ferulic acid, the first from the curry spice turmeric and the second a major constituent of fruit and vegetables, are candidates in this regard. Not only do these compounds serve as antioxidants but, in addition, they are strong inducers of the heat-shock response. Food supplementation with curcumin and ferulic acid are therefore being considered as a novel nutritional approach to reduce oxidative damage and amyloid pathology in AD. We review here some of the emerging concepts of pathways to neurodegeneration and how these may be overcome by a nutritional approach.},
author = {Calabrese, Vittorio and Guagliano, Eleonora and Sapienza, Maria and Panebianco, Mariangela and Calafato, Stella and Puleo, Edoardo and Pennisi, Giovanni and Mancuso, Cesare and {Allan Butterfield}, D. and Stella, Annamaria Giuffrida},
doi = {10.1007/s11064-006-9203-y},
issn = {0364-3190},
journal = {Neurochemical Research},
keywords = {Aging,Aging: metabolism,Alzheimer Disease,Alzheimer Disease: genetics,Alzheimer Disease: metabolism,Animals,Gene Expression,Heme Oxygenase (Decyclizing),Heme Oxygenase (Decyclizing): metabolism,Humans,Longevity,Longevity: genetics,Neurodegenerative Diseases,Neurodegenerative Diseases: genetics,Neurodegenerative Diseases: physiopathology,Oxidation-Reduction,Oxidative Stress,Oxidative Stress: genetics,Oxidative Stress: physiology,Reactive Oxygen Species,Reactive Oxygen Species: metabolism,Thioredoxins,Thioredoxins: metabolism},
mendeley-groups = {curcumin},
month = dec,
number = {4-5},
pages = {757--773},
pmid = {17191135},
title = {{Redox Regulation of Cellular Stress Response in Aging and Neurodegenerative Disorders: Role of Vitagenes}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17191135},
volume = {32},
year = {2006}
}
</bibtex>

[2]
<bibtex>
@article{Suh2007,
abstract = {Glutamate induces cell death by upsetting the cellular redox homeostasis, termed oxidative glutamate toxicity, in a mouse hippocampal cell line, HT22. Extracellular signal-regulated kinases (ERK) 1/2 are known key players in this process. Here we characterized the roles of both MAP kinases and cell cycle regulators in mediating oxidative glutamate toxicity and the neuroprotective mechanisms of curcumin in HT22 cells. c-Jun N-terminal kinase (JNK) and p38 kinase were activated during the glutamate-induced HT22 cell death, but at a later stage than ERK activation. Treatment with a JNK inhibitor, SP600125, or a p38 kinase inhibitor, SB203580, partly attenuated this cell death. Curcumin, a natural inhibitor of JNK signaling, protected the HT22 cells from glutamate-induced death at nanomolar concentrations more efficiently than SP600125. These doses of curcumin affected neither the level of intracellular glutathione nor the level of reactive oxygen species, but inactivated JNK and p38 significantly. Moreover, curcumin markedly upregulated a cell-cycle inhibitory protein, p21cip1, and downregulated cyclin D1 levels, which might help the cell death prevention. Our results suggest that curcumin has a neuroprotective effect against oxidative glutamate toxicity by inhibiting MAP kinase signaling and influencing cell-cycle regulation.},
author = {Suh, Hyun-Woo and Kang, Seongman and Kwon, Ki-Sun},
doi = {10.1007/s11010-006-9365-6},
issn = {0300-8177},
journal = {Molecular and cellular biochemistry},
keywords = {Animals,Anthracenes,Anthracenes: pharmacology,Antioxidants,Antioxidants: metabolism,Cell Death,Cell Death: drug effects,Cell Line,Curcumin,Curcumin: pharmacology,Cyclin D1,Cyclin D1: metabolism,Cyclin-Dependent Kinase Inhibitor p21,Cyclin-Dependent Kinase Inhibitor p21: metabolism,Glutamic Acid,Glutamic Acid: toxicity,Glutathione,Glutathione: metabolism,JNK Mitogen-Activated Protein Kinases,JNK Mitogen-Activated Protein Kinases: antagonists,MAP Kinase Signaling System,MAP Kinase Signaling System: drug effects,Mice,Neuroprotective Agents,Neuroprotective Agents: pharmacology,Oxidative Stress,Oxidative Stress: drug effects,Phosphorylation,Phosphorylation: drug effects,Reactive Oxygen Species,Reactive Oxygen Species: metabolism,Transcription Factor AP-1,Transcription Factor AP-1: metabolism},
mendeley-groups = {curcumin},
month = apr,
number = {1-2},
pages = {187--94},
pmid = {17131042},
title = {{Curcumin attenuates glutamate-induced HT22 cell death by suppressing MAP kinase signaling.}},
url = {http://www.ncbi.nlm.nih.gov/pubmed/17131042},
volume = {298},
year = {2007}
}
</bibtex>