Itoero Posted May 30, 2017 Share Posted May 30, 2017 The polyglutamine (polyQ) diseases are a group of neurodegenerative disorders caused by expanded cytosine-adenine-guanine (CAG) repeats encoding a long polyQ tract in the respective proteins. To date, a total of nine polyQ disorders have been described: six spinocerebellar ataxias (SCA) types 1, 2, 6, 7, 17; Machado-Joseph disease (MJD/SCA3); Huntington's disease (HD); dentatorubral pallidoluysian atrophy (DRPLA); and spinal and bulbar muscular atrophy, X-linked 1 (SMAX1/SBMA). I have spinocerebellar ataxia type 7. https://www.ncbi.nlm.nih.gov/pubmed/24816443 Your ribosomes form polyglutamine tracts in certain proteins which causes the proteins to bind and become toxic/harmful. Glutamine is the most abundant naturally occurring, nonessential amino acid in the human body, and one of the few amino acids that can directly cross the bloodbrain barrier. Humans obtain glutamine through catabolism of proteins in foods they eat. As brunch I eat milk+brinta+proteinpowder+sugar. Brinta is wheat and contains a lot of gluten, which contains glutamine. Protein powder contains also a lot of glutamine. Is it wise to reduce the amount of glutamine I consume? Or is this effect negligible? If people with a PolyQ disease don't consume any glutamine...can the disease still manifest? They found antigliadin antibodies in people with Huntington's disease and cerebellar ataxia. https://www.ncbi.nlm.nih.gov/pubmed/14718716 https://www.ncbi.nlm.nih.gov/pubmed/17951282 Is it possible that this is not a real gluten sensitivity but can those anti gliadin antibodies be a reaction on the long polyQ tract in certain proteins which cause the disease? Link to comment Share on other sites More sharing options...
Itoero Posted June 25, 2017 Author Share Posted June 25, 2017 Trehalose is synthesized as a stress-responsive factor when cells are exposed to environmental stresses likeheat, cold, oxidation, desiccation, and so forth...but it's not present in mammals. They found that Trehalose alleviates polyglutamine-mediated pathology. It seems like it causes inhibition of polyglutamine-induced protein aggregation...it's this aggregation that causes proteins to be harmful and it causes the polyglutamine (polyQ) diseases. They have tested it on mice and people with Huntington and people with spinocerebellar ataxia type3. https://www.ncbi.nlm.nih.gov/pubmed/14730359 https://www.ncbi.nlm.nih.gov/pubmed/24587280 http://www.raredr.com/news/bioblasts-trehalose-stabilizes-spinocerebellar-ataxia-symptoms Link to comment Share on other sites More sharing options...
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