Evidence map›Paper›PMID 28072416›Full record

ArticleTranslational psychiatry2017

Preclinical amyloid pathology biomarker positivity: effects on tau pathology and neurodegeneration.

K Höglund, S Kern, A Zettergren, A Börjesson-Hansson, H Zetterberg, I Skoog, K Blennow

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
5.9field-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

46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

K HöglundClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, Centre for ageing and Health, AgeCap, University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
S KernClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, Centre for ageing and Health, AgeCap, University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
A ZettergrenClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, Centre for ageing and Health, AgeCap, University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
A Börjesson-HanssonClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, Centre for ageing and Health, AgeCap, University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
H ZetterbergClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, Centre for ageing and Health, AgeCap, University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
I SkoogClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, Centre for ageing and Health, AgeCap, University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
K BlennowClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, The Sahlgrenska Academy, Centre for ageing and Health, AgeCap, University of Gothenburg, Sahlgrenska University Hospital, Mölndal, Sweden.
Sahlgrenska University Hospital · SEUniversity of Gothenburg · SENational Hospital for Neurology and Neurosurgery · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain autopsy and biomarker studies indicate that the pathology of Alzheimer's disease (AD) is initiated at least 10-20 years before clinical symptoms. This provides a window of opportunity to initiate preventive treatment. However, this emphasizes the necessity for biomarkers that identify individuals at risk for developing AD later in life. In this cross-sectional study, originating from three epidemiologic studies in Sweden (n=1428), the objective was to examine whether amyloid pathology, as determined by low cerebrospinal fluid (CSF) concentration of the 42 amino acid form of β-amyloid (Aβ42), is associated with biomarker evidence of other pathological changes in cognitively healthy elderly. A total of 129 patients were included and CSF levels of Aβ42, total tau, tau phosphorylated at threonine 181 (p-tau), neurogranin, VILIP-1, VEGF, FABP3, Aβ40, neurofilament light, MBP, orexin A, BDNF and YKL-40 were measured. Among these healthy elderly, 35.6% (N=46) had CSF Aβ42 levels below 530 pg ml

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesApolipoprotein E4BiomarkersBrain-Derived Neurotrophic FactorChitinase-3-Like Protein 1Cross-Sectional StudiesFatty Acid Binding Protein 3FemaleHealthy VolunteersHumansMaleMyelin Basic ProteinNeurocalcinAmyloid beta-Peptidesamyloid beta-protein (1-42)Apolipoprotein E4BDNF protein, humanBiomarkersBrain-Derived Neurotrophic FactorCHI3L1 protein, humanChitinase-3-Like Protein 1FABP3 protein, humanFatty Acid Binding Protein 3MAPT protein, humanMyelin Basic ProteinNeurocalcinneurofilament protein LNeurofilament ProteinsNeurograninOrexinsPeptide FragmentsPhosphoproteinstau ProteinsVascular Endothelial Growth Factor AVEGFA protein, humanVSNL1 protein, human

Identifiers

PMID28072416
PMCPMC5545720
OpenAlexW2571225994

What OpenQuestion holds

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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.