Chelating Labile Iron In Parkinson's Disease
ironjustice
Redox imbalance in Parkinson's disease
Biochimica et Biophysica Acta (BBA) - General Subjects, Volume 1780,
Issue 11, November 2008, Pages 1362-1367
Shankar J. Chinta, Julie K. Andersen
Parkinson's disease (PD) is an adult-onset neurodegenerative disorder
characterized by preferential loss of dopaminergic neurons in an area
of the midbrain called the substantia nigra (SN) along with occurrence
of intraneuronal inclusions called Lewy bodies.
The majority of cases of PD are sporadic in nature with late onset
(95% of patients); however a few PD cases (5%) are seen in familial
clusters with generally earlier onset.
Although PD has been heavily researched, so far the exact cause of the
rather selective cell death is unknown.
Multiple lines of evidence suggest an important role for oxidative
stress. Dopaminergic neurons (DA) are particularly prone to oxidative
stress due to DA metabolism and auto-oxidation combined with increased
iron, decreased total glutathione levels and mitochondrial complex I
inhibition-induced ROS production in the SN which can lead to cell
death by exceeding the oxidative capacity of DA-containing cells in
the region.
Enhancing antioxidant capabilities and chelating labile iron pools in
this region therefore constitutes a rational approach to prevent or
slow ongoing damage of DA neurons.
In this review, we summarize the various sources of reactive oxygen
species that may cause redox imbalance in PD as well as potential
therapeutic targets for attenuation of oxidative stress associated
with PD.
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