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Neurochem Res. 2009 Oct;34(10):1838-46. doi: 10.1007/s11064-009-9986-8. Epub 2009 May 15.

Modulation of alpha-synuclein aggregation by dopamine: a review.

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  • 1Department of Pathology, Bio21 Molecular Science and Biotechnology Institute, The University of Melbourne, Parkville, VIC 3010, Australia.


Parkinson's disease (PD) is a progressive neurodegenerative disorder that is characterized by (1) the selective loss of dopaminergic neurons in the substantia nigra and (2) the deposition of misfolded alpha-synuclein (alpha-syn) as amyloid fibrils in the intracellular Lewy bodies in various region of the brain. Current thinking suggests that an interaction between alpha-syn and dopamine (DA) leads to the selective death of neuronal cells and the accumulation of misfolded alpha-syn. However, the exact mechanism by which this occurs is not fully defined. DA oxidation could play a key role is the pathogenesis of PD by causing oxidative stress, mitochondria dysfunction and impairment of protein metabolism. Here, we review the literature on the role of DA and its oxidative intermediates in modulating the aggregation pathways of alpha-syn.

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