Evidence map›Paper›PMID 31167811›Full record

ArticleJournal of neurology, neurosurgery, and psychiatry2019

CSF biomarkers distinguish idiopathic normal pressure hydrocephalus from its mimics.

Anna Jeppsson, Carsten Wikkelsö, Kaj Blennow, Henrik Zetterberg, Radu Constantinescu, Anne M Remes, Sanna-Kaisa Herukka, Tuomas Rauramaa, Katarina Nagga, Ville Leinonen and 1 more

Registry-linked trialOpen access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neurology, neurosurgery, and psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05915000 (Alterations of CSF Protein Markers as Prognostic Indicator of the Response to Cerebrospinal Fluid Shunting in Chronic Hydrocephalus in Adults), which is not on this map. Cited by 52 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 3 pooled it
5.4field-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.

NCT05915000 recruitingnot on this map

Alterations of CSF Protein Markers as Prognostic Indicator of the Response to Cerebrospinal Fluid Shunting in Chronic Hydrocephalus in Adults

TypeobservationalSponsorUniversity of ValenciaRan2019 to 2029Enrolled150ConditionsBeta-amiloid and Phospho-tau Proteins in CSF, Ventricular Size After CSF Shunt, Cognitive Impairment and CSF Shunt, Motor Impairment Evolution After CSF ShuntArmsLumbar CSF protein marker determination
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 3 syntheses or guidelines pooled it, 93 citations in OpenAlex.

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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

11 authors at 5 institutions in 3 countries.

Anna JeppssonHydrocephalus Research Unit, Department of clinical neuroscience, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden anna.jeppsson@gu.se.ORCID 0000-0002-5908-1904
Carsten WikkelsöHydrocephalus Research Unit, Department of clinical neuroscience, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Radu ConstantinescuDepartment of Clinical Neuroscience, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Anne M RemesUnit of Clinical Neuroscience, Neurology, University of Oulu, Oulu, Finland.
Sanna-Kaisa HerukkaDepartment of Neurology, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland.
Tuomas RauramaaDepartment of Pathology, Kuopio University Hospital and University of Eastern Finland, Kuopio, Finland.
Katarina NaggaDepartment of Acute Internal Medicine and Geriatrics, Linköping University, Linköping, Sweden.
Ville LeinonenMedical Research Center, Oulu University Hospital, Oulu, Finland.
Mats TullbergHydrocephalus Research Unit, Department of clinical neuroscience, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0003-4997-5266
University of Gothenburg · SEUniversity of Eastern Finland · FISahlgrenska University Hospital · SELinköping University · SEOulu University Hospital · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo examine the differential diagnostic significance of cerebrospinal fluid (CSF) biomarkers reflecting Alzheimer's disease-related amyloid β (Aβ) production and aggregation, cortical neuronal damage, tau pathology, damage to long myelinated axons and astrocyte activation, which hypothetically separates patients with idiopathic normal pressure hydrocephalus (iNPH) from patients with other neurodegenerative disorders.

methodsThe study included lumbar CSF samples from 82 patients with iNPH, 75 with vascular dementia, 70 with Parkinson's disease, 34 with multiple system atrophy, 34 with progressive supranuclear palsy, 15 with corticobasal degeneration, 50 with Alzheimer's disease, 19 with frontotemporal lobar degeneration and 54 healthy individuals (HIs). We analysed soluble amyloid precursor protein alpha (sAPPα) and beta (sAPPβ), Aβ species (Aβ38, Aβ40 and Aβ42), total tau (T-tau), phosphorylated tau, neurofilament light and monocyte chemoattractant protein 1 (MCP-1).

resultsPatients with iNPH had lower concentrations of tau and APP-derived proteins in combination with elevated MCP-1 compared with HI and the non-iNPH disorders. T-tau, Aβ40 and MCP-1 together yielded an area under the curve of 0.86, differentiating iNPH from the other disorders. A prediction algorithm consisting of T-tau, Aβ40 and MCP-1 was designed as a diagnostic tool using CSF biomarkers.

conclusionsThe combination of the CSF biomarkers T-tau, Aβ40 and MCP-1 separates iNPH from cognitive and movement disorders with good diagnostic sensitivity and specificity. This may have important implications for diagnosis and clinical research on disease mechanisms for iNPH.

Indexed as

Diagnosis, DifferentialAgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorBiomarkersCase-Control StudiesChemokine CCL2Dementia, VascularFemaleFrontotemporal Lobar DegenerationHumansHydrocephalus, Normal PressureMaleMiddle AgedAmyloid beta-Peptidesamyloid beta-protein (1-40)amyloid beta-protein (1-42)Amyloid beta-Protein PrecursorAPP protein, humanBiomarkersCCL2 protein, humanChemokine CCL2MAPT protein, humanneurofilament protein LNeurofilament ProteinsPeptide FragmentsPhosphoproteinstau ProteinsAlzheimer’s diseasebiomarkerscorticobasal degenerationCSFfrontotemporal dementiaidiopathic normal pressure hydrocephalusMultiple systems atrophyParkinson’s diseaseProgressive supranuclear palsyvascular dementia

Identifiers

PMID31167811
PMCPMC6817981
OpenAlexW2949014264

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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.