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Review

Using ‘omics’ to define pathogenesis and biomarkers of Parkinson’s disease

, , , &
Pages 925-942 | Published online: 09 Jan 2014
 

Abstract

Although great effort has been put forth to uncover the complex molecular mechanisms exploited in the pathogenesis of Parkinson’s disease, a satisfactory explanation remains to be discovered. The emergence of several -omics techniques, transcriptomics, proteomics and metabolomics, have been integral in confirming previously identified pathways that are associated with dopaminergic neurodegeneration and subsequently Parkinson’s disease, including mitochondrial and proteasomal function and synaptic neurotransmission. Additionally, these unbiased techniques, particularly in the brain regions uniquely associated with the disease, have greatly enhanced our ability to identify novel pathways, such as axon-guidance, that are potentially involved in Parkinson’s pathogenesis. A comprehensive appraisal of the results obtained by different -omics has also reconfirmed the increase in oxidative stress as a common pathway likely to be critical in Parkinson’s development/progression. It is hoped that further integration of these techniques will yield a more comprehensive understanding of Parkinson’s disease etiology and the biological pathways that mediate neurodegeneration.

Financial & competing interests disclosure

The effort of the authors was supported by the National Institutes of Health grants (ES004696, NS057567, AG025327, AG033398, NS060252, ES016873 and NS062684) as well as grants from the Michael J Fox Foundation. W Michael Caudle is supported by award number K99ES017477 from the National Institute of Environmental Health Science. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

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