Evidence map›Paper›PMID 30526557›Full record

ArticleBMC neurology2018

Transient increase in CSF GAP-43 concentration after ischemic stroke.

Åsa Sandelius, Nicholas C Cullen, Åsa Källén, Lars Rosengren, Crister Jensen, Vesna Kostanjevecki, Manu Vandijck, Henrik Zetterberg, Kaj Blennow

Open access · goldAbstract read
In one paragraph

Article in BMC neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.9field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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  5. Article
  6. Review
  7. Review
  8. Biofluid biomarkers for Alzheimer's disease.Frontiers in aging neuroscience · 2024
    Review
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  15. Proteomic Analysis of Rhesus Macaque Brain Explants Treated WithFrontiers in cellular and infection microbiology · 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

9 authors at 4 institutions in 5 countries.

Åsa SandeliusInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. sandelius.asa@gmail.com.ORCID http://orcid.org/0000-0001-9771-4840
Nicholas C CullenInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Åsa KällénClinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
Lars RosengrenInstitute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation, The Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Crister JensenInstitute of Clinical Sciences, University of Gothenburg, Gothenburg, Sweden.
Vesna KostanjeveckiFujirebio Europe nv, Ghent, Belgium.
Manu VandijckFujirebio Europe nv, Ghent, Belgium.
Henrik ZetterbergInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
Kaj BlennowInstitute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. kaj.blennow@neuro.gu.se.
Sahlgrenska University Hospital · SEFujirebio (Belgium) · BEUniversity of Gothenburg · SEUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCerebrospinal fluid (CSF) biomarkers reflect ongoing processes in the brain. Growth-associated protein 43 (GAP-43) is highly upregulated in brain tissue shortly after experimental ischemia suggesting the CSF GAP-43 concentration may be altered in ischemic brain disorders. CSF GAP-43 concentration is elevated in Alzheimer's disease patients; however, patients suffering from stroke have not been studied previously.

methodsThe concentration of GAP-43 was measured in longitudinal CSF samples from 28 stroke patients prospectively collected on days 0-1, 2-4, 7-9, 3 weeks, and 3-5 months after ischemia and cross-sectionally in 19 controls. The stroke patients were clinically evaluated using a stroke severity score system. The extent of the brain lesion, including injury size and degrees of white matter lesions and atrophy were evaluated by CT and magnetic resonance imaging.

resultsIncreased GAP-43 concentration was detected from day 7-9 to 3 weeks after stroke, compared to day 1-4 and to levels in the control group (P = 0.02 and P = 0.007). At 3-5 months after stroke GAP-43 returned to admission levels. The initial increase in GAP-43 during the nine first days was associated to stroke severity, the degree of white matter lesions and atrophy and correlated positively with infarct size (r

conclusionsThe transient increase of CSF GAP-43 is important to take into account when used as a biomarker for other neurodegenerative diseases such as Alzheimer's disease. Furthermore, GAP-43 may be a marker of neuronal responses after stroke and additional studies confirming the potential of CSF GAP-43 to reflect severity and outcome of stroke in larger cohorts are warranted.

Indexed as

AgedAlzheimer DiseaseAtrophyBiomarkersBrainBrain IschemiaFemaleGAP-43 ProteinHumansLongitudinal StudiesMagnetic Resonance ImagingMaleMiddle AgedProspective StudiesStrokeBiomarkersGAP-43 ProteinBiomarkersCerebrospinal fluidGAP-43NeurodegenerationStroke

Identifiers

PMID30526557
PMCPMC6284302
OpenAlexW2904035061

What OpenQuestion holds

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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.