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Abnormalities in actin assembly have been linked to cellular death in other studies, including polyglutamine induced neuronal dysfunction. By analogy it seems that the actin dysfunction documented for FA patients may be a key contributory factor to neuronal cell death. However, glutathionylation of other proteins may also contribute.Thus, consistent with the decreased content of reduced GSH in FA patient samples, a global increase in Cobicistat protein glutathionylation has been reported in FA samples. Foods such as spinach, asparagus, and avocado contain mg quantities of GSH. Unfortunately, consuming large quantities of these foods likely does not change the levels of GSH in the body.The mechanisms for the increases in GSH are unclear since they might be due to a variety of factors, including increased transcriptional activity of proteins used to Fluocinolone acetonide synthesize GSH, increased translational activity, decreased degradation of GSH, increased reduction of GSSG, increased transport of precursors, etc.Curcumin has been reported to induce an increase in both mRNA and protein levels of glutamatecysteine ligase. The mRNA and protein increases were attributed to changes in transcription factor binding capacities in immortalized bronchial epithelial cells. Whether analogous mechanisms are responsible for the observed increases in GSH levels in brain tissue remains to be determined.Nevertheless, all three compounds have been reported to display some protection in vivo in various neurodegenerative disease models, including PD. Increasing GSH content represents one therapeutic strategy for treating neurodegenerative diseases, and while oral intake of GSH does not increase GSH levels in the body, it has become apparent that small molecules can induce changes in GSH content in animal models.The studies cited above provide limited examples of natural agents taken orally with potential protective effects for neurodegenerative diseases, possibly through modulation of GSH levels in the brain.Such studies on natural inducers of GSH are continuing and much remains to be learned about their efficacy and mechanisms of action.As discussed above, oral GSH does not increase levels of GSH in the body; however, intravenous dosing of GSH apparently does. PD patients were given mg GSH twice daily for days.Sechi stated that research had shown that GSH does pass through the BBB. Therefore, while a specific transport mechanism has been proposed for GSH through the BBB, skepticism regarding the quantitative impact of that transport mechanism is warranted, as discussed above.Nevertheless, GSH itself would not have to cross the BBB to promote an increase in intracellular GSH content.Thus, precursors of GSH in the blood could lead to an increase in total GSH in the brain.Hence additional studies are warranted to distinguish the relative efficiency of GSH and its precursors to supplement the GSH content of neurons without eliciting toxic effects.Nacetylcysteine as a GSH precursorwhile two clinical studies using intravenous GSH injection have shown opposing results, studies with NAC as a cysteineGSH precursor have shown promising results in mice in both PD and AD models. As discussed above, these results have led to ongoing clinical trials investigating the effects of NAC, which is already a FDA approved drug, in combination with other nutraceuticals for treatment of AD.

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