Evidence map›Paper›PMID 29513680›Full record

ArticlePloS one2018

Augmented frontal cortex diacylglycerol levels in Parkinson's disease and Lewy Body Disease.

Paul L Wood, Soumya Tippireddy, Joshua Feriante, Randall L Woltjer

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.8field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 74 citations in OpenAlex.

  1. Cellular and systemic modifiers of alpha-synuclein proteostasis.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
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  4. Plasma Metabolomics Profiles in Prodromal and Clinical Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
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  19. Coordinated modification in expression levels of HSPA1A/B, DGKH, and NOTCH2 in Parkinson's patients' blood and substantia nigra as a diagnostic sign: the transcriptomes' relationship.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023
    Article
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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

4 authors at 2 institutions in 1 country.

Paul L WoodMetabolomics Unit, College of Veterinary Medicine, Lincoln Memorial University, Cumberland Gap Pkwy., Harrogate, TN, United States of America.ORCID 0000-0002-5853-9936
Soumya TippireddyDeBusk College of Osteopathic Medicine, Lincoln Memorial University, Cumberland Gap Pkwy., Harrogate, TN, United States of America.
Joshua FerianteDeBusk College of Osteopathic Medicine, Lincoln Memorial University, Cumberland Gap Pkwy., Harrogate, TN, United States of America.
Randall L WoltjerDepartment of Neurology, Oregon Health Science University and Portland VA Medical Center, Portland, OR, United States of America.
Lincoln Memorial University · USPortland VA Medical Center · US

Funding

Outreach, Recruitment and Education CoreP30AG008017 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI DODGE, HIROKO HAYAMA · 1990 to 2019
$27.7M
NIA NIH HHS P30 AG008017NIH HHS AG08017
6 · The paper itself

Abstract

backgroundResearch from our laboratory, and that of other investigators, has demonstrated augmented levels of diacylglycerols (DAG) in the frontal cortex and plasma of subjects with Alzheimer's disease (AD) and Mild Cognitive Impairment (MCI). We have extended these observations to investigate the frontal cortex of subjects with Parkinson's disease (PD) and Lewy Body Disease (LBD), with and without coexisting pathologic features of AD. METHODS/PRINCIPAL

findingsUtilizing a high-resolution mass spectrometry analytical platform, we clearly demonstrate that DAG levels are significantly increased in the frontal cortex of subjects with PD, LBD with intermediate neocortical AD neuropathology, and in LBD with established neocortical AD neuropathology. In the case of the PD cohort, increases in cortical DAG levels were detected in cases with no neocortical pathology but were greater in subjects with neocortical pathology. These data suggest that DAG changes occur early in the disease processes and are amplified as cortical dysfunction becomes more established.

conclusionsThese findings suggest that altered DAG synthesis/metabolism is a common feature of neurodegenerative diseases, characterized by proteinopathy, that ultimately result in cognitive deficits. With regard to the mechanism responsible for these biochemical alterations, selective decrements in cortical levels of phosphatidylcholines in LBD and PD suggest that augmented degradation and/or decreased synthesis of these structural glycerophospholipids may contribute to increases in the pool size of free DAGs. The observed augmentation of DAG levels may be phospholipase-driven since neuroinflammation is a consistent feature of all disease cohorts. If this conclusion can be validated it would support utilizing DAG levels as a biomarker of the early disease process and the investigation of early intervention with anti-inflammatory agents.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseBiomarkersDiglyceridesFemaleFrontal LobeHumansLewy Body DiseaseMaleMiddle AgedNeocortexNeurodegenerative DiseasesParkinson DiseaseBiomarkersDiglycerides

Identifiers

PMID29513680
PMCPMC5841652
OpenAlexW2789783533

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LicenceCC BY
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Registered trials

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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.