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School of Medical Sciences, College of Life Sciences and Medicine, University of Aberdeen, Aberdeen, UK
1 Correspondence: School of Medical Sciences, College of Life Sciences and Medicine, University of Aberdeen, Aberdeen, AB25 2ZD, Scotland, UK. E-mail: p.teismann{at}abdn.ac.uk
Parkinsons disease (PD) is the second most common neurodegenerative disease, affecting over a million people in the United States alone, and is characterized by rigidity, bradykinesia, resting tremor, and postural instability. Its main neuropathological feature is the loss of dopaminergic neurons of the substantia nigra pars compacta. However, the pathogenesis of this loss is not understood fully. One of the earliest biochemical changes seen in PD is a reduction in the levels of total glutathione, a key cellular antioxidant. Traditionally, it has been thought that this decrease in GSH levels is the consequence of increased oxidative stress, a process heavily implicated in PD pathogenesis. However, emerging evidence suggests that GSH depletion may itself play an active role in PD pathogenesis. This review aims to explore the contribution of GSH depletion to PD pathogenesis.—Martin, H. L., Teismann, P. Glutathione—a review on its role and significance in Parkinsons disease.
Key Words: oxidative stress complex I ubiquitin-proteasome inflammation incidental Lewy body disease
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