Mitochondrial proteomics as a selective tool for unraveling Parkinson’s disease pathogenesis
@article{Pienaar2010MitochondrialPA, title={Mitochondrial proteomics as a selective tool for unraveling Parkinson’s disease pathogenesis}, author={Ilse S. Pienaar and David T Dexter and Pierre R. Burkhard}, journal={Expert Review of Proteomics}, year={2010}, volume={7}, pages={205 - 226} }
Parkinson’s disease (PD) is a neurodegenerative disease characterized by the large-scale loss of dopaminergic neurons in the substantia nigra and the formation of protein aggregates that accumulate in the cytoplasm of the remaining dopaminergic neurons. Most cases arise sporadically, while the precise cause remains obscure. This lack of understanding as to the etiology of PD continues to serve as a major barrier for delivering effective therapeutics. Mitochondria are potent integrators and…
19 Citations
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The present review summarizes the major advances in the field of PD research in humans utilizing proteomic techniques and potential samples for proteomic analysis and limitations associated with the analyses of different types of samples have also been discussed.
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This review describes several quantitative studies of proteins from mitochondria isolated by centrifugation, separated by various methods, and analyzed by advanced mass spectrometry, illustrating the methods by showing that multiple pathways and networks are affected in cells from patients carrying gene variations affecting a mitochondrial protein.
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The extensive efforts to rapidly obtain differentially expressed proteomes and unravel the redox proteomic status in mitochondria have yielded clinical insights into the neuropathological mechanisms of disease, identification of disease early stage and evaluation of disease progression.
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Current understanding concerning the proteins involved in structural and functional changes that affect synaptic contact-points in PD are reviewed and the need for developing therapeutics aimed at deregulated protein synthesis and degradation pathways operating at axonal and dendritic synapses for preserving “normal” circuitry and function is emphasized.
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