Evidence map›Paper›PMID 28341600›Full record

ReviewBrain research bulletin2017

Metabolic Dysfunction in Parkinson's Disease: Bioenergetics, Redox Homeostasis and Central Carbon Metabolism.

Annadurai Anandhan, Maria S Jacome, Shulei Lei, Pablo Hernandez-Franco, Aglaia Pappa, Mihalis I Panayiotidis, Robert Powers, Rodrigo Franco

Open access · greenAbstract readReview
In one paragraph

Review in Brain research bulletin, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 papers.

0numbers the graph read from it
0cells of the map it votes in
99citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

99 citing papers in PubMed, 163 citations in OpenAlex.

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39 more citing papers are in PubMed but not listed here.

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

8 authors at 3 institutions in 3 countries.

Annadurai AnandhanSchool of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE 68516, United States; Redox Biology Center, University of Nebraska-Lincoln, Lincoln, NE 68503, United States.
Maria S JacomeSchool of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE 68516, United States.
Shulei LeiDepartment of Chemistry, University of Nebraska-Lincoln, Lincoln, NE 68503, United States.
Pablo Hernandez-FrancoSchool of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE 68516, United States; Redox Biology Center, University of Nebraska-Lincoln, Lincoln, NE 68503, United States.
Aglaia PappaDepartment of Molecular Biology and Genetics, Democritus University of Thrace, University Campus, Dragana, 68100 Alexandroupolis, Greece.
Mihalis I PanayiotidisSchool of Life Sciences, Heriot-Watt University, Edinburgh EH14 4AS, Scotland, UK.
Robert PowersRedox Biology Center, University of Nebraska-Lincoln, Lincoln, NE 68503, United States; Department of Chemistry, University of Nebraska-Lincoln, Lincoln, NE 68503, United States.
Rodrigo FrancoSchool of Veterinary Medicine and Biomedical Sciences, University of Nebraska-Lincoln, Lincoln, NE 68516, United States; Redox Biology Center, University of Nebraska-Lincoln, Lincoln, NE 68503, United States. Electronic address: rfrancocruz2@unl.edu.
University of Nebraska–Lincoln · USDemocritus University of Thrace · GRHeriot-Watt University · GB

Funding

THE REDOX-MEDIATED REGULATION OF IRON-RESPONSIVE GENE EXPRESSION IN LIVERP20RR017675 · NCRR · UNIVERSITY OF NEBRASKA LINCOLN · PI BECKER, DONALD F · 2002 to 2011
$20.4M
Redox Biology CenterP30GM103335 · NIGMS · UNIVERSITY OF NEBRASKA LINCOLN · PI BECKER, DONALD F · 2012 to 2016
$4.3M
NCRR NIH HHS P20 RR017675NIGMS NIH HHS P30 GM103335
6 · The paper itself

Abstract

The loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and the accumulation of protein inclusions (Lewy bodies) are the pathological hallmarks of Parkinson's disease (PD). PD is triggered by genetic alterations, environmental/occupational exposures and aging. However, the exact molecular mechanisms linking these PD risk factors to neuronal dysfunction are still unclear. Alterations in redox homeostasis and bioenergetics (energy failure) are thought to be central components of neurodegeneration that contribute to the impairment of important homeostatic processes in dopaminergic cells such as protein quality control mechanisms, neurotransmitter release/metabolism, axonal transport of vesicles and cell survival. Importantly, both bioenergetics and redox homeostasis are coupled to neuro-glial central carbon metabolism. We and others have recently established a link between the alterations in central carbon metabolism induced by PD risk factors, redox homeostasis and bioenergetics and their contribution to the survival/death of dopaminergic cells. In this review, we focus on the link between metabolic dysfunction, energy failure and redox imbalance in PD, making an emphasis in the contribution of central carbon (glucose) metabolism. The evidence summarized here strongly supports the consideration of PD as a disorder of cell metabolism.

Indexed as

BrainBrain Diseases, MetabolicCarbonDopaminergic NeuronsEnergy MetabolismHomeostasisHumansMitochondriaOxidation-ReductionOxidative StressParkinson DiseaseSubstantia NigraCarbonBioenergeticsGlucoseGlycolysisMitochondriaNeurodegenerationOxidative stressTCA cycle

Identifiers

PMID28341600
PMCPMC5555796
OpenAlexW2602703797

What OpenQuestion holds

Textmetadata
LicenceTDM
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.