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Biomolecules 2015, 5(2), 1122-1142; doi:10.3390/biom5021122

Interaction between Neuromelanin and Alpha-Synuclein in Parkinson’s Disease

1,2
and
1,2,*
1
Beijing Institute of Geriatrics, Xuanwu Hospital of Capital University of Medical Sciences, No.45 changchun St., Xicheng District, Beijing 100053, China
2
Parkinson's disease Center of Beijing Institute for Brain Disorders, Beijing 100053, China
*
Author to whom correspondence should be addressed.
Academic Editor: Stephan N. Witt
Received: 15 March 2015 / Accepted: 29 April 2015 / Published: 5 June 2015
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Abstract

Parkinson’s disease (PD) is a very common neurodegenerative disorder characterized by the accumulation of α-synuclein (α-syn) into Lewy body (LB) inclusions and the loss of neuronmelanin (NM) containing dopamine (DA) neurons in the substantia nigra (SN). Pathological α-syn and NM are two prominent hallmarks in this selective and progressive neurodegenerative disease. Pathological α-syn can induce dopaminergic neuron death by various mechanisms, such as inducing oxidative stress and inhibiting protein degradation systems. Therefore, to explore the factors that trigger α-syn to convert from a non-toxic protein to toxic one is a pivotal question to clarify the mechanisms of PD pathogenesis. Many triggers for pathological α-syn aggregation have been identified, including missense mutations in the α-syn gene, higher concentration, and posttranslational modifications of α-Syn. Recently, the role of NM in inducing α-syn expression and aggregation has been suggested as a mechanism for this pigment to modulate neuronal vulnerability in PD. NM may be responsible for PD and age-associated increase and aggregation in α-syn. Here, we reviewed our previous study and other recent findings in the area of interaction between NM and α-syn. View Full-Text
Keywords: alpha-synuclein; Parkinson’s disease; neuromelanin; oxidative stress alpha-synuclein; Parkinson’s disease; neuromelanin; oxidative stress
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Xu, S.; Chan, P. Interaction between Neuromelanin and Alpha-Synuclein in Parkinson’s Disease. Biomolecules 2015, 5, 1122-1142.

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