REMEMBER: Never try something based on some random internet comment. Always talk to a doctor about your research and ideas before trying anything new.
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So, today's discovery is a supplement long discussed in the Parkinson's community. The wonderful aspect of this supplement is that it has a human study to go along with it's animal research:
N-Acetyl Cysteine May Support Dopamine Neurons in Parkinson's Disease: Preliminary Clinical and Cell Line Data
journals.plos.org/plosone/a...
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I know, I know . . . people with SCA do not have dopamine issues, but this molecule appears to be a powerful antioxidant and that is very relevant to many neurological disorders:
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"NAC is an over-the-counter antioxidant supplement and also is available as an injectable pharmaceutical that protects the liver in cases of acetaminophen overdose. Our cell line study is consistent with other laboratory studies that have suggested how NAC might have a beneficial effect in neurodegenerative disorders such as PD. For example, older studies showed that cotreatment with NAC rescued rat pheochromocytoma cells from the toxic effect of dopamine combined with buthionine sulfoximine, an inhibitor of gamma-glutamyl transpeptidase, or phoron a substrate of glutathione transferase [37]. A more recent study showed that NAC may reduce misfolded protein levels and ameliorate proteotoxicity through heat shock proteins."
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That last sentence takes you to this study:
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N-Acetyl cysteine blunts proteotoxicity in a heat shock protein-dependent manner
ncbi.nlm.nih.gov/pubmed/?te....
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In that study they found:
"We measured heat shock protein 70 (Hsp70) levels because Hsp70 is a protective chaperone that helps refold proteins or guides ubiquitinated proteins toward degradation by the proteasome. Hsp70 levels were higher in MG132-treated cells when N-acetyl cysteine was applied. . . . These data reveal a new role for N-acetyl cysteine: this compound may reduce misfolded protein levels and ameliorate proteotoxicity through heat shock proteins. These findings broaden the potential mechanisms of action for this dietary supplement in neurodegenerative proteinopathies."
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And, why is that important? Because:
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"The neuroprotective effects of G-CSF may be produced by increases in Hsp70, Beclin-1, LC3-II and the p-ERK survival pathway. Upregulation of chaperone and autophagy levels further enhances the clearance of mutant protein aggregation, slowing the progression of pathology in SCA17 mice. Therefore, we showed that the early intervention of G-CSF has a neuroprotective effect, delaying the progression of SCA17 in mutant mice via increases in the levels of chaperone expression and autophagy."
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Targeting the prodromal stage of spinocerebellar ataxia type 17 mice: G-CSF in the prevention of motor deficits via upregulating chaperone and autophagy levels.
ncbi.nlm.nih.gov/pubmed/269...
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Peripheral Oxidative Stress Biomarkers in Spinocerebellar Ataxia Type 3/Machado-Joseph Disease
ncbi.nlm.nih.gov/pubmed/289...
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In other words animal models of SCA3 and SCA17 show that a reduction in oxidative stress helps make them better, and that is exactly what NAC appears to do, and it's this simple little protein sold on Amazon:
amazon.com/Life-Extension-N...
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Wow!
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Joe
Partial Possible Treatment for some SCAs.
CoQ10 (ubiquinone).
