Selected Papers from 1st International Electronic Conference on Metabolomics

A special issue of Metabolites (ISSN 2218-1989).

Deadline for manuscript submissions: closed (30 April 2017)

Special Issue Editors


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Department of Anesthesiology and Pain Medicine, Northwest Metabolomics Research Center, University of Washington, Seattle, WA, USA
Interests: metabolite profiling; metabolite method development; disease diagnostics; systems biology; NMR spectroscopy; mass spectrometry
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Metabolomics, Proteomics and Mass Spectrometry Cores, University of Utah, Salt Lake City, UT 84112, USA
Interests: yeast metabolism; iron and copper metabolism; metabolomics core; secondary metabolism in antibiotic producing bacteria

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Institute of Functional Genomics, University of Regensburg, Am BioPark 9, 93053 Regensburg, Germany
Interests: metabolomics; small molecule analysis; separation science; hyphenated mass spectrometry; sample preparation for metabolomics; cancer
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Sussex Research Laboratories, Inc., 100, Sussex Drive, Ottawa, ON K1A OR6, Canada
Interests: small molecule structure determination; NMR; separation science

Special Issue Information

Dear Colleagues,

This Special Issue will collect some selected, invited and contributed talks during the 1st International Electronic Conference on Metabolomics (IECM-1) which was supported by the Metabolites journal, website http://sciforum.net/conference/iecm-1.

Prof. Dr. Daniel Raftery
Prof. Dr. Daniel Raftery
Prof. Dr. James Cox
Dr. Katja Dettmer
Dr. Adrian S. Culf
Guest Editors

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Published Papers (1 paper)

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Metabolic Investigations of the Molecular Mechanisms Associated with Parkinson’s Disease
by Robert Powers, Shulei Lei, Annadurai Anandhan, Darrell D. Marshall, Bradley Worley, Ronald L. Cerny, Eric D. Dodds, Yuting Huang, Mihalis I. Panayiotidis, Aglaia Pappa and Rodrigo Franco
Metabolites 2017, 7(2), 22; https://doi.org/10.3390/metabo7020022 - 24 May 2017
Cited by 42 | Viewed by 8042
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by fibrillar cytoplasmic aggregates of α-synuclein (i.e., Lewy bodies) and the associated loss of dopaminergic cells in the substantia nigra. Mutations in genes such as α-synuclein (SNCA) account for only 10% of PD [...] Read more.
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by fibrillar cytoplasmic aggregates of α-synuclein (i.e., Lewy bodies) and the associated loss of dopaminergic cells in the substantia nigra. Mutations in genes such as α-synuclein (SNCA) account for only 10% of PD occurrences. Exposure to environmental toxicants including pesticides and metals (e.g., paraquat (PQ) and manganese (Mn)) is also recognized as an important PD risk factor. Thus, aging, genetic alterations, and environmental factors all contribute to the etiology of PD. In fact, both genetic and environmental factors are thought to interact in the promotion of idiopathic PD, but the mechanisms involved are still unclear. In this study, we summarize our findings to date regarding the toxic synergistic effect between α-synuclein and paraquat treatment. We identified an essential role for central carbon (glucose) metabolism in dopaminergic cell death induced by paraquat treatment that is enhanced by the overexpression of α-synuclein. PQ “hijacks” the pentose phosphate pathway (PPP) to increase NADPH reducing equivalents and stimulate paraquat redox cycling, oxidative stress, and cell death. PQ also stimulated an increase in glucose uptake, the translocation of glucose transporters to the plasma membrane, and AMP-activated protein kinase (AMPK) activation. The overexpression of α-synuclein further stimulated an increase in glucose uptake and AMPK activity, but impaired glucose metabolism, likely directing additional carbon to the PPP to supply paraquat redox cycling. Full article
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