Evidence map›Paper›PMID 26121274›Full record

ArticleAmyotrophic lateral sclerosis & frontotemporal degeneration2015

The longitudinal cerebrospinal fluid metabolomic profile of amyotrophic lateral sclerosis.

Elizabeth Gray, James R Larkin, Tim D W Claridge, Kevin Talbot, Nicola R Sibson, Martin R Turner

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Amyotrophic lateral sclerosis & frontotemporal degeneration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.0field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 51 citations in OpenAlex.

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  13. NR1D1 downregulation in astrocytes induces a phenotype that is detrimental to cocultured motor neurons.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
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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

6 authors at 1 institution in 1 country.

Elizabeth Graya Nuffield Department of Clinical Neuroscience , University of Oxford , Oxford , UK.
James R Larkinb Cancer Research UK and Medical Research Council, Oxford Institute for Radiation Oncology, Department of Oncology , University of Oxford , Oxford , UK.
Tim D W Claridgec Department of Chemistry , University of Oxford , Oxford , UK.
Kevin Talbota Nuffield Department of Clinical Neuroscience , University of Oxford , Oxford , UK.
Nicola R Sibsonb Cancer Research UK and Medical Research Council, Oxford Institute for Radiation Oncology, Department of Oncology , University of Oxford , Oxford , UK.
Martin R Turnera Nuffield Department of Clinical Neuroscience , University of Oxford , Oxford , UK.
University of Oxford · GB

Funding

Cancer Research UK 16945Medical Research Council G0701923Medical Research Council MR/K01014X/1Motor Neurone Disease Association TURNER/JAN13/944-795
6 · The paper itself

Abstract

Neurochemical biomarkers are urgently sought in ALS. Metabolomic analysis of cerebrospinal fluid (CSF) using proton nuclear magnetic resonance ((1)H-NMR) spectroscopy is a highly sensitive method capable of revealing nervous system cellular pathology. The (1)H-NMR CSF metabolomic signature of ALS was sought in a longitudinal cohort. Six-monthly serial collection was performed in ALS patients across a range of clinical sub-types (n = 41) for up to two years, and in healthy controls at a single time-point (n = 14). A multivariate statistical approach, partial least squares discriminant analysis, was used to determine differences between the NMR spectra from patients and controls. Significantly predictive models were found using those patients with at least one year's interval between recruitment and the second sample. Glucose, lactate, citric acid and, unexpectedly, ethanol were the discriminating metabolites elevated in ALS. It is concluded that (1)H-NMR captured the CSF metabolomic signature associated with derangements in cellular energy utilization connected with ALS, and was most prominent in comparisons using patients with longer disease duration. The specific metabolites identified support the concept of a hypercatabolic state, possibly involving mitochondrial dysfunction specifically. Endogenous ethanol in the CSF may be an unrecognized novel marker of neuronal tissue injury in ALS.

Indexed as

AgedAmyotrophic Lateral SclerosisBiomarkersCase-Control StudiesCitric AcidCohort StudiesDiscriminant AnalysisDisease ProgressionEthanolFemaleGlucoseHumansLactic AcidLongitudinal StudiesMaleMetabolomicsBiomarkersCitric AcidEthanolGlucoseLactic Acidbiomarkermotor neuron diseaseneurochemicalNuclear magnetic resonanceproton

Identifiers

PMID26121274
PMCPMC4720042
OpenAlexW1708297083

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.