Evidence map›Paper›PMID 26856756›Full record

Trial reportScientific reports2016

Cerebral white matter lesions - associations with Aβ isoforms and amyloid PET.

Danielle van Westen, Daniel Lindqvist, Kaj Blennow, Lennart Minthon, Katarina Nägga, Erik Stomrud, Henrik Zetterberg, Oskar Hansson

Registry-linked trialOpen access · goldAbstract readClinical Trial
PubMed Full text at PMC Publisher
In one paragraph

Trial report in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01208675 (The Swedish BioFINDER Study), which is not on this map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.6field-weighted citation impact, top 4% 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.

NCT01208675 completednot on this map

The Swedish BioFINDER Study: Early Diagnosis of Alzheimer's Disease - a Multidisciplinary Approach

TypeobservationalSponsorSkane University HospitalRan2010 to 2024Enrolled1,150ConditionsMild Cognitive Impairment, Alzheimer's Disease, Dementia With Lewy Bodies, Vascular Dementia
3 · Its place in the literature

Who cites it

44 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Considerations in the clinical use of amyloid PET and CSF biomarkers for Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
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  20. Review
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

8 authors at 4 institutions in 2 countries.

Danielle van WestenDiagnostic Radiology, Department of Clinical Sciences Lund, Lund University.
Daniel LindqvistPsychiatry, Department of Clinical Sciences Lund, Lund University, Lund, Sweden.
Kaj BlennowClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Lennart MinthonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden.
Katarina NäggaClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden.
Erik StomrudClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden.
Henrik ZetterbergClinical Neurochemistry Laboratory, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at University of Gothenburg, Mölndal, Sweden.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences Malmö, Lund University, Sweden.
Lund University · SESkåne University Hospital · SEUniversity College London · GBUniversity of Gothenburg · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Small vessel disease (SVD) and amyloid deposition may promote each other, with a potential association between SVD and altered production or clearance of β-amyloid (Aβ) affecting its cleavage products. We investigated the relationship between SVD, multiple isoforms of Aβ in cerebrospinal fluid (CSF) and cortical Aβ in 831 subjects with cognitive performance ranging from normal to Alzheimer's disease (AD) (the Swedish BioFINDER study). SVD was estimated as white matter lesions (WML) and lacunes. 18F-flutemetamol PET was performed in 321 subjects. Lower CSF levels of Aβ38 and Aβ40 were consistently associated with increased WML in all subgroups, while lower levels of CSF Aβ42 were associated with WML mainly in AD. CSF Aβ38 and Aβ40 were associated with regional WML in all regions, while CSF Aβ42 was associated with temporal WML only. A composite measure of 18F-flutemetamol uptake was not associated with WML, and regional 18F-flutemetamol uptake only with temporal WML. Lacunes were not associated with Aβ isoforms nor 18F-flutemetamol uptake. Our results suggest that WML may be associated with alterations in the production or clearance of Aβ species, particularly of Aβ38 and Aβ40. However, in AD cases, Aβ42 pathology might be associated with WML, especially in the temporal lobe.

Indexed as

Alzheimer DiseasePositron-Emission TomographyTemporal LobeWhite MatterAgedAged, 80 and overAmyloid beta-PeptidesAniline CompoundsBenzothiazolesFemaleHumansMaleMiddle AgedProtein IsoformsAmyloid beta-PeptidesAniline CompoundsBenzothiazolesflutemetamolProtein Isoforms

Identifiers

PMID26856756
PMCPMC4746584
OpenAlexW2394753565

What OpenQuestion holds

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LicenceCC BY
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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.