Evidence map›Paper›PMID 30075734›Full record

ArticleAlzheimer's research & therapy2018

The EMIF-AD PreclinAD study: study design and baseline cohort overview.

Elles Konijnenberg, Stephen F Carter, Mara Ten Kate, Anouk den Braber, Jori Tomassen, Chinenye Amadi, Linda Wesselman, Hoang-Ton Nguyen, Jacoba A van de Kreeke, Maqsood Yaqub and 17 more

Open access · goldAbstract readTwin Study
In one paragraph

Article in Alzheimer's research & therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

50 citing papers in PubMed, 85 citations in OpenAlex.

  1. Quantitative amyloid PET in Alzheimer's disease: the AMYPAD prognostic and natural history study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2020
    Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Contributions of amyloid beta and cerebral small vessel disease in clinical decline.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  18. Article
  19. Performance of a [Neurology · 2023
    Article
  20. Observational
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

27 authors at 3 institutions in 2 countries.

Elles KonijnenbergAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands. e.konijnenberg@vumc.nl.ORCID 0000-0002-2962-2941
Stephen F CarterWolfson Molecular Imaging Centre, Division of Neuroscience and Experimental Psychology, University of Manchester, Manchester, UK.
Mara Ten KateAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Anouk den BraberAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Jori TomassenAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Chinenye AmadiWolfson Molecular Imaging Centre, Division of Neuroscience and Experimental Psychology, University of Manchester, Manchester, UK.
Linda WesselmanAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Hoang-Ton NguyenDepartment of Ophthalmology, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Jacoba A van de KreekeDepartment of Ophthalmology, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Maqsood YaqubDepartment of Radiology & Nuclear Medicine, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Matteo DemuruAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Sandra D MulderNeurochemistry Laboratory, Department of Clinical Chemistry, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Arjan HillebrandDepartment of Clinical Neurophysiology, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Femke H BouwmanAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Charlotte E TeunissenNeurochemistry Laboratory, Department of Clinical Chemistry, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Erik H SernéDepartment of Internal Medicine, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Annette C MollDepartment of Ophthalmology, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Frank D VerbraakDepartment of Ophthalmology, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Rainer HinzWolfson Molecular Imaging Centre, Division of Informatics, Imaging and Data Sciences, Faculty of Medicine, Biology and Health, University of Manchester, Manchester, UK.
Neil PendletonWolfson Molecular Imaging Centre, Division of Neuroscience and Experimental Psychology, University of Manchester, Manchester, UK.
Adriaan A LammertsmaDepartment of Radiology & Nuclear Medicine, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Bart N M van BerckelDepartment of Radiology & Nuclear Medicine, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Frederik BarkhofDepartment of Radiology & Nuclear Medicine, VU University Medical Center, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Dorret I BoomsmaDepartment of Biological Psychology, VU University, Neuroscience Amsterdam, Amsterdam, The Netherlands.
Philip ScheltensAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Karl HerholzWolfson Molecular Imaging Centre, Division of Neuroscience and Experimental Psychology, University of Manchester, Manchester, UK.
Pieter Jelle VisserAlzheimer Center, Department of Neurology, VU University Medical Center, Neuroscience Amsterdam, PO Box 7057, 1007 MB, Amsterdam, The Netherlands.
Amsterdam Neuroscience · NLUniversity of Manchester · GBMaastricht University · NL

Funding

EU/EFPIA Innovative Medicines Initiative Joint Undertaking EMIF grant agreement n°115372
6 · The paper itself

Abstract

backgroundAmyloid pathology is the pathological hallmark in Alzheimer's disease (AD) and can precede clinical dementia by decades. So far it remains unclear how amyloid pathology leads to cognitive impairment and dementia. To design AD prevention trials it is key to include cognitively normal subjects at high risk for amyloid pathology and to find predictors of cognitive decline in these subjects. These goals can be accomplished by targeting twins, with additional benefits to identify genetic and environmental pathways for amyloid pathology, other AD biomarkers, and cognitive decline.

methodsFrom December 2014 to October 2017 we enrolled cognitively normal participants aged 60 years and older from the ongoing Manchester and Newcastle Age and Cognitive Performance Research Cohort and the Netherlands Twins Register. In Manchester we included single individuals, and in Amsterdam monozygotic twin pairs. At baseline, participants completed neuropsychological tests and questionnaires, and underwent physical examination, blood sampling, ultrasound of the carotid arteries, structural and resting state functional brain magnetic resonance imaging, and dynamic amyloid positron emission tomography (PET) scanning with [

resultsWe included 285 participants, who were on average 74.8 ± 9.7 years old, 64% female. Fifty-eight participants (22%) had an abnormal amyloid PET scan.

conclusionsA rich baseline dataset of cognitively normal elderly individuals has been established to estimate risk factors and biomarkers for amyloid pathology and future cognitive decline.

Indexed as

AgedAged, 80 and overAge FactorsAlzheimer DiseaseAmyloid beta-PeptidesAniline CompoundsApolipoproteins EBenzothiazolesCarotid ArteriesCognition DisordersCohort StudiesFemaleHumansImaging, Three-DimensionalInternational CooperationMagnetic Resonance ImagingAmyloid beta-PeptidesAniline CompoundsApolipoproteins EBenzothiazolesflutemetamol[18F]flutemetamolAmyloidCognitively normalMonozygotic twinsPreclinical Alzheimer’s disease

Identifiers

PMID30075734
PMCPMC6091034
OpenAlexW2886692233

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.