Glutathione

a review on its role and significance in Parkinson's disease

Heather L Martin, Peter Teismann

Research output: Contribution to journalArticle

181 Citations (Scopus)

Abstract

Parkinson's 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.
Original languageEnglish
Pages (from-to)3263-3272
Number of pages10
JournalThe FASEB Journal
Volume23
Issue number10
Early online date19 Jun 2009
DOIs
Publication statusPublished - Oct 2009

Fingerprint

Glutathione
Parkinson Disease
Neurodegenerative diseases
Hypokinesia
Oxidative stress
Dopaminergic Neurons
Tremor
Rigidity
Neurodegenerative Diseases
Neurons
Oxidative Stress
Antioxidants

Keywords

  • glutathione
  • humans
  • Parkinson disease
  • oxidative stress
  • complex I
  • ubiquitin-proteasome
  • incidental Lewy body disease
  • inflammation

Cite this

Glutathione : a review on its role and significance in Parkinson's disease. / Martin, Heather L; Teismann, Peter.

In: The FASEB Journal, Vol. 23, No. 10, 10.2009, p. 3263-3272.

Research output: Contribution to journalArticle

Martin, Heather L ; Teismann, Peter. / Glutathione : a review on its role and significance in Parkinson's disease. In: The FASEB Journal. 2009 ; Vol. 23, No. 10. pp. 3263-3272.
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