Central nervous system uptake of intranasal glutathione in Parkinson’s disease

Glutathione (GSH) is depleted early in the course of Parkinson’s disease (PD), and deficiency has been shown to perpetuate oxidative stress, mitochondrial dysfunction, impaired autophagy, and cell death. GSH repletion has been proposed as a therapeutic intervention. The objective of this study was t...

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Published in:NPJ Parkinson's Disease 2016-02, Vol.2 (1), p.16002-16002, Article 16002
Main Authors: Mischley, Laurie K, Conley, Kevin E, Shankland, Eric G, Kavanagh, Terrance J, Rosenfeld, Michael E, Duda, John E, White, Collin C, Wilbur, Timothy K, De La Torre, Prysilla U, Padowski, Jeannie M
Format: Article
Language:English
Subjects:
692/308/153
692/617
692/700/565/1436
Biomedical and Life Sciences
Biomedicine
Neurology
Neurosciences
Parkinson's disease
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Summary:Glutathione (GSH) is depleted early in the course of Parkinson’s disease (PD), and deficiency has been shown to perpetuate oxidative stress, mitochondrial dysfunction, impaired autophagy, and cell death. GSH repletion has been proposed as a therapeutic intervention. The objective of this study was to evaluate whether intranasally administered reduced GSH, (in)GSH, is capable of augmenting central nervous system GSH concentrations, as determined by magnetic resonance spectroscopy in 15 participants with mid-stage PD. After baseline GSH measurement, 200 mg (in)GSH was self-administered inside the scanner without repositioning, then serial GSH levels were obtained over ~1 h. Statistical significance was determined by one-way repeated measures analysis of variance. Overall, (in)GSH increased brain GSH relative to baseline ( P
ISSN:2373-8057
2373-8057
DOI:10.1038/npjparkd.2016.2