Evidence map›Paper›PMID 28826181›Full record

ArticleJournal of Alzheimer's disease : JAD2017

Detecting At-Risk Alzheimer's Disease Cases.

Tormod Fladby, Lene Pålhaugen, Per Selnes, Knut Waterloo, Geir Bråthen, Erik Hessen, Ina Selseth Almdahl, Kjell-Arne Arntzen, Eirik Auning, Carl Fredrik Eliassen and 17 more

Abstract readMulticenter Study
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 5 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

44 citing papers in PubMed, 5 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
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  5. Pooled it
  6. Trial
  7. Interpreting p-tau217 on the ward: frailty and plasma biomarkers in acutely admitted older adults.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
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  11. Repeated plasma p-tau217 measurements to monitor clinical progression heterogeneity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

27 authors.

Tormod FladbyDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Lene PålhaugenDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Per SelnesDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Knut WaterlooDepartment of Neurology, University Hospital of North Norway, Tromsø, Norway.
Geir BråthenDepartment of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
Erik HessenDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Ina Selseth AlmdahlDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Kjell-Arne ArntzenDepartment of Neurology, University Hospital of North Norway, Tromsø, Norway.
Eirik AuningDepartment of Geriatric Psychiatry, Akershus University Hospital, Lørenskog, Norway.
Carl Fredrik EliassenDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Ragna EspenesDepartment of Neurology, University Hospital of North Norway, Tromsø, Norway.
Ramune GrambaiteDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Gøril Rolfseng GrøntvedtDepartment of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
Krisztina Kunszt JohansenDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Stein Harald JohnsenDepartment of Neurology, University Hospital of North Norway, Tromsø, Norway.
Lisa Flem KalheimDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Bjørn-Eivind KirsebomDepartment of Neurology, University Hospital of North Norway, Tromsø, Norway.
Kai Ivar MüllerDepartment of Neurology and National Neuromuscular Centre, University Hospital of North Norway, Tromsø, Norway.
Arne Exner NaklingInstitute of Clinical Medicine, University of Bergen, Bergen, Norway.
Arvid RongveDepartment of Research and Innovation, Haugesund Hospital, Helse Fonna, Haugesund, Norway.
Sigrid Botne SandoDepartment of Neuromedicine and Movement Science, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology, Trondheim, Norway.
Nikias SiafarikasDepartment of Geriatric Psychiatry, Akershus University Hospital, Lørenskog, Norway.
Ane Løvli StavDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Sandra TecelaoThe Intervention Centre, Oslo University Hospital, Oslo, Norway.
Santiago TimonDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.
Svein Ivar BekkelundDepartment of Neurology and National Neuromuscular Centre, University Hospital of North Norway, Tromsø, Norway.
Dag AarslandDepartment of Neurology, Akershus University Hospital, Lørenskog, Norway.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While APOEɛ4 is the major genetic risk factor for Alzheimer's disease (AD), amyloid dysmetabolism is an initial or early event predicting clinical disease and is an important focus for secondary intervention trials. To improve identification of cases with increased AD risk, we evaluated recruitment procedures using pathological CSF concentrations of Aβ42 (pAβ) and APOEɛ4 as risk markers in a multi-center study in Norway. In total, 490 subjects aged 40-80 y were included after response to advertisements and media coverage or memory clinics referrals. Controls (n = 164) were classified as normal controls without first-degree relatives with dementia (NC), normal controls with first-degree relatives with dementia (NCFD), or controls scoring below norms on cognitive screening. Patients (n = 301) were classified as subjective cognitive decline or mild cognitive impairment. Subjects underwent a clinical and cognitive examination and MRI according to standardized protocols. Core biomarkers in CSF from 411 and APOE genotype from 445 subjects were obtained. Cases (both self-referrals (n = 180) and memory clinics referrals (n = 87)) had increased fractions of pAβ and APOEɛ4 frequency compared to NC. Also, NCFD had higher APOEɛ4 frequencies without increased fraction of pAβ compared to NC, and cases recruited from memory clinics had higher fractions of pAβ and APOEɛ4 frequency than self-referred. This study shows that memory clinic referrals are pAβ enriched, whereas self-referred and NCFD cases more frequently are pAβ negative but at risk (APOEɛ4 positive), suitable for primary intervention.

Indexed as

Alzheimer DiseaseAdultAgedAged, 80 and overAmyloid beta-PeptidesApolipoprotein E4Cognition DisordersDisease ProgressionFemaleHumansMaleMiddle AgedNeuropsychological TestsNorwayPeptide FragmentsPsychiatric Status Rating ScalesAmyloid beta-Peptidesamyloid beta-protein (1-42)Apolipoprotein E4Peptide FragmentsAlzheimer’s diseaseamyloidapolipoprotein E4biomarkerscerebrospinal fluidmild cognitive impairmentsubjective cognitive decline

Identifiers

PMID28826181
PMCPMC5611830

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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.