Evidence map›Paper›PMID 28535786›Full record

ReviewBMC neurology2017

Biochemical markers in vascular cognitive impairment associated with subcortical small vessel disease - A consensus report.

A Wallin, E Kapaki, M Boban, S Engelborghs, D M Hermann, B Huisa, M Jonsson, M G Kramberger, L Lossi, B Malojcic and 12 more

Abstract readReviewConsensus Statement
PubMed Full text at PMC Publisher
In one paragraph

Review in BMC neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

45 citing papers in PubMed, 1 synthesis or guideline pooled it.

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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

22 authors.

A WallinDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden. anders.wallin@neuro.gu.se.ORCID http://orcid.org/0000-0001-9506-0513
E Kapaki1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
M BobanDepartment of Neurology, University Hospital Centre Zagreb, Medical School, University of Zagreb, Zagreb, Croatia.
S EngelborghsMemory Clinic and Department of Neurology, Hospital Network Antwerp (ZNA) Middelheim and HogeBeuken, Antwerp, Belgium.
D M HermannDepartment of Neurology, University Hospital Essen, Essen, Germany.
B HuisaDepartment of Neurology, University of California, Irvine, California, USA.
M JonssonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
M G KrambergerDepartment of Neurology, University Medical Center Ljubljana, Ljubljana, Slovenia.
L LossiDepartment of Veterinary Sciences, University of Turin, Turin, Italy.
B MalojcicDepartment of Neurology, University Hospital Centre Zagreb, Medical School, University of Zagreb, Zagreb, Croatia.
S MehrabianDepartment of Neurology, University Hospital "Alexandrovska", Medical University, Sofia, Bulgaria.
A MerighiDepartment of Veterinary Sciences, University of Turin, Turin, Italy.
E B Mukaetova-LadinskaInstitute of Neuroscience, Campus for Ageing and Vitality, Newcastle University, Newcastle upon Tyne, NE4 5PL, UK.
G P Paraskevas1st Department of Neurology, Eginition Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
B O PopescuDepartment of Neurology, Colentina Clinical Hospital, School of Medicine, 'Carol Davila' University of Medicine and Pharmacy, Bucharest, Romania.
R RavidBrain Bank Consultants, Amsterdam, The Netherlands.
L TraykovDepartment of Neurology, University Hospital "Alexandrovska", Medical University, Sofia, Bulgaria.
G Tsivgoulis2nd Department of Neurology, Attikon Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
G WeinsteinSchool of Public Health, University of Haifa, Haifa, Israel.
A KorczynDepartment of Neurology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
M BjerkeReference Center for Biological Markers of Dementia, Department of Biomedical Sciences, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium.
G RosenbergUniversity of New Mexico Health Sciences Center, Albuquerque, NM, 87131, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVascular cognitive impairment (VCI) is a heterogeneous entity with multiple aetiologies, all linked to underlying vascular disease. Among these, VCI related to subcortical small vessel disease (SSVD) is emerging as a major homogeneous subtype. Its progressive course raises the need for biomarker identification and/or development for adequate therapeutic interventions to be tested. In order to shed light in the current status on biochemical markers for VCI-SSVD, experts in field reviewed the recent evidence and literature data.

methodThe group conducted a comprehensive search on Medline, PubMed and Embase databases for studies published until 15.01.2017. The proposal on current status of biochemical markers in VCI-SSVD was reviewed by all co-authors and the draft was repeatedly circulated and discussed before it was finalized.

resultsThis review identifies a large number of biochemical markers derived from CSF and blood. There is a considerable overlap of VCI-SSVD clinical symptoms with those of Alzheimer's disease (AD). Although most of the published studies are small and their findings remain to be replicated in larger cohorts, several biomarkers have shown promise in separating VCI-SSVD from AD. These promising biomarkers are closely linked to underlying SSVD pathophysiology, namely disruption of blood-CSF and blood-brain barriers (BCB-BBB) and breakdown of white matter myelinated fibres and extracellular matrix, as well as blood and brain inflammation. The leading biomarker candidates are: elevated CSF/blood albumin ratio, which reflects BCB/BBB disruption; altered CSF matrix metalloproteinases, reflecting extracellular matrix breakdown; CSF neurofilment as a marker of axonal damage, and possibly blood inflammatory cytokines and adhesion molecules. The suggested SSVD biomarker deviations contrasts the characteristic CSF profile in AD, i.e. depletion of amyloid beta peptide and increased phosphorylated and total tau.

conclusionsCombining SSVD and AD biomarkers may provide a powerful tool to identify with greater precision appropriate patients for clinical trials of more homogeneous dementia populations. Thereby, biomarkers might promote therapeutic progress not only in VCI-SSVD, but also in AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorBiomarkersBlood-Brain BarrierCognitive DysfunctionDementiaHumansVascular DiseasesWhite MatterAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAPP protein, humanBiomarkersAlzheimer’s diseaseBiomarkersBloodCSFDementiaMixed type dementiaSubcortical small vessel diseaseVascular cognitive impairment

Identifiers

PMID28535786
PMCPMC5442599

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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.