Evidence map›Paper›PMID 28620826›Full record

ArticleNeuromolecular medicine2017

Individual Amino Acid Supplementation Can Improve Energy Metabolism and Decrease ROS Production in Neuronal Cells Overexpressing Alpha-Synuclein.

Vedad Delic, Jeddidiah W D Griffin, Sandra Zivkovic, Yumeng Zhang, Tam-Anh Phan, Henry Gong, Dale Chaput, Christian Reynes, Vinh B Dinh, Josean Cruz and 8 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neuromolecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 25% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 23 citations in OpenAlex.

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  13. Redox Regulation and Oxidative Stress in Mammalian Oocytes and Embryos DevelopedInternational journal of environmental research and public health · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 4 institutions in 1 country.

Vedad DelicDepartment of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL, 35233, USA.
Jeddidiah W D GriffinDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Sandra ZivkovicDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Yumeng ZhangDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Tam-Anh PhanDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Henry GongDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA.
Dale ChaputDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Christian ReynesDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Vinh B DinhDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Josean CruzDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Eni CvitkovicDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Devon PlacidesDepartment of Pharmaceutical Science, University of South Florida, Tampa, FL, 33613, USA.
Ernide FredericDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Hamed MirzaeiDavis School of Gerontology, University of Southern California, Los Angeles, CA, 90089, USA.
Stanley M StevensDepartment of Cell Biology, Microbiology and Molecular Biology, University of South Florida, Tampa, FL, 33620, USA.
Umesh JinwalDepartment of Pharmaceutical Science, University of South Florida, Tampa, FL, 33613, USA.
Daniel C LeeDepartment of Pharmaceutical Science, University of South Florida, Tampa, FL, 33613, USA.
Patrick C BradshawDepartment of Biomedical Sciences, Quillen College of Medicine, East Tennessee State University, Johnson City, TN, 37614, USA. bradshawp@etsu.edu.ORCID http://orcid.org/0000-0002-4591-6798
University of South Florida · USEast Tennessee State University · USUniversity of Alabama at Birmingham · USUniversity of Southern California · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is a neurodegenerative disorder characterized by alpha-synuclein accumulation and loss of dopaminergic neurons in the substantia nigra (SN) region of the brain. Increased levels of alpha-synuclein have been shown to result in loss of mitochondrial electron transport chain complex I activity leading to increased reactive oxygen species (ROS) production. WT alpha-synuclein was stably overexpressed in human BE(2)-M17 neuroblastoma cells resulting in increased levels of an alpha-synuclein multimer, but no increase in alpha-synuclein monomer levels. Oxygen consumption was decreased by alpha-synuclein overexpression, but ATP levels did not decrease and ROS levels did not increase. Treatment with ferrous sulfate, a ROS generator, resulted in decreased oxygen consumption in both control and alpha-synuclein overexpressing cells. However, this treatment only decreased ATP levels and increased ROS production in the cells overexpressing alpha-synuclein. Similarly, paraquat, another ROS generator, decreased ATP levels in the alpha-synuclein overexpressing cells, but not in the control cells, further demonstrating how alpha-synuclein sensitized the cells to oxidative insult. Proteomic analysis yielded molecular insights into the cellular adaptations to alpha-synuclein overexpression, such as the increased abundance of many mitochondrial proteins. Many amino acids and citric acid cycle intermediates and their ester forms were individually supplemented to the cells with L-serine, L-proline, L-aspartate, or L-glutamine decreasing ROS production in oxidatively stressed alpha-synuclein overexpressing cells, while diethyl oxaloacetate or L-valine supplementation increased ATP levels. These results suggest that dietary supplementation with individual metabolites could yield bioenergetic improvements in PD patients to delay loss of dopaminergic neurons.

Indexed as

Adenosine Triphosphatealpha-SynucleinAmino AcidsCell Line, TumorCulture MediaDrug Evaluation, PreclinicalEnergy MetabolismFerrous CompoundsHumansMitochondriaNeuroblastomaNeuronsOxidative StressOxygen ConsumptionParaquatReactive Oxygen SpeciesAdenosine Triphosphatealpha-SynucleinAmino AcidsCulture MediaFerrous Compoundsferrous sulfateParaquatReactive Oxygen SpeciesRecombinant ProteinsAlpha-synucleinAmino acidsCitric acid cycleIronMetabolic therapyMitochondrialParkinson’s diseaseProteomics

Identifiers

PMID28620826
OpenAlexW2626520328

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.