Evidence map›Paper›PMID 24300239›Full record

ArticleNeurobiology of aging2014

Dysregulation of glucose metabolism is an early event in sporadic Parkinson's disease.

Laura Dunn, George Fg Allen, Adamantios Mamais, Helen Ling, Abi Li, Kate E Duberley, Iain P Hargreaves, Simon Pope, Janice L Holton, Andrew Lees and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Neurobiology of aging, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed
6.5field-weighted citation impact, top 3% 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

126 citing papers in PubMed, 251 citations in OpenAlex.

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  6. Neuromodulatory control of energy reserves in dopaminergic neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  17. Parkinson's disease and glucose metabolism impairment.Translational neurodegeneration · 2025
    Review
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  20. Article

66 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

12 authors at 3 institutions in 1 country.

Laura DunnReta Lila Weston Laboratories, UCL Institute of Neurology, London, UK. Electronic address: laura.dunn11@uclmail.net.
George Fg AllenMRC Protein Phosphorylation Unit. University of Dundee, Dundee, UK.
Adamantios MamaisReta Lila Weston Laboratories, UCL Institute of Neurology, London, UK.
Helen LingReta Lila Weston Laboratories, UCL Institute of Neurology, London, UK; Queen Square Brain Bank, UCL Institute of Neurology, London, UK.
Abi LiQueen Square Brain Bank, UCL Institute of Neurology, London, UK.
Kate E DuberleyDepartment of Molecular Neuroscience, UCL Institute of Neurology, London, UK; Neurometabolic Unit, National Hospital for Neurology and Neurosurgery, London, UK.
Iain P HargreavesNeurometabolic Unit, National Hospital for Neurology and Neurosurgery, London, UK.
Simon PopeNeurometabolic Unit, National Hospital for Neurology and Neurosurgery, London, UK.
Janice L HoltonQueen Square Brain Bank, UCL Institute of Neurology, London, UK.
Andrew LeesReta Lila Weston Laboratories, UCL Institute of Neurology, London, UK.
Simon J HealesChemical Pathology Department, Great Ormond Street Hospital, London, UK; Clinical and Molecular Genetics Unit, UCL Institute of Child Health, London, UK; Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Rina BandopadhyayReta Lila Weston Laboratories, UCL Institute of Neurology, London, UK.
University College London · GBMRC Protein Phosphorylation and Ubiquitylation Unit · GBNational Hospital for Neurology and Neurosurgery · GB

Funding

Medical Research Council MC_G1000735Wellcome Trust 089698
6 · The paper itself

Abstract

Unlike most other cell types, neurons preferentially metabolize glucose via the pentose phosphate pathway (PPP) to maintain their antioxidant status. Inhibiting the PPP in neuronal cell models causes cell death. In rodents, inhibition of this pathway causes selective dopaminergic cell death leading to motor deficits resembling parkinsonism. Using postmortem human brain tissue, we characterized glucose metabolism via the PPP in sporadic Parkinson's disease (PD), Alzheimer's disease (AD), and controls. AD brains showed increased nicotinamide adenine dinucleotide phosphate (NADPH) production in areas affected by disease. In PD however, increased NADPH production was only seen in the affected areas of late-stage cases. Quantifying PPP NADPH-producing enzymes glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase by enzyme-linked immunosorbent assay, showed a reduction in the putamen of early-stage PD and interestingly in the cerebellum of early and late-stage PD. Importantly, there was no decrease in enzyme levels in the cortex, putamen, or cerebellum of AD. Our results suggest that down-regulation of PPP enzymes and a failure to increase antioxidant reserve is an early event in the pathogenesis of sporadic PD.

Indexed as

AgedAged, 80 and overAnimalsAntioxidantsCell DeathCerebellumDopaminergic NeuronsFemaleGlucoseGlucosephosphate DehydrogenaseHumansMaleNADPNeuronsParkinson DiseasePentose Phosphate PathwayAntioxidantsGlucoseGlucosephosphate DehydrogenaseNADPPhosphogluconate DehydrogenaseGlucose metabolismNADPHNeurodegenerationParkinson's diseasePentose-phosphate pathway

Identifiers

PMID24300239
PMCPMC3969149
OpenAlexW2034532609

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.