Evidence map›Paper›PMID 24639435›Full record

ArticleJournal of neurology, neurosurgery, and psychiatry2014

Apolipoprotein E ε2 genotype delays onset of dementia with Lewy bodies in a Norwegian cohort.

Guro Berge, Sigrid B Sando, Arvid Rongve, Dag Aarsland, Linda R White

Open access · hybridAbstract read
In one paragraph

Article in Journal of neurology, neurosurgery, and psychiatry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
5.0field-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.

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

43 citing papers in PubMed, 81 citations in OpenAlex.

  1. Article
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  4. APOE ε4 linked effects on clinical features and neuropathology in dementia with Lewy bodies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  5. Article
  6. An Update on Neuroaging on Earth and in Spaceflight.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Apolipoprotein E Gene in α-Synucleinopathies: A Narrative Review.International journal of molecular sciences · 2024
    Review
  9. Review
  10. medRxiv : the preprint server for health sciences · 2023
    Article
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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

5 authors at 3 institutions in 2 countries.

Guro BergeFaculty of Medicine, Department of Neuroscience, Norwegian University of Science and Technology (NTNU), Trondheim, Norway.
Sigrid B SandoFaculty of Medicine, Department of Neuroscience, Norwegian University of Science and Technology (NTNU), Trondheim, Norway Department of Neurology, University Hospital of Trondheim, Trondheim, Norway.
Arvid RongveDepartment of Psychiatry, Haugesund Hospital, Haugesund, Norway.
Dag AarslandDepartment of Neurobiology, Care Sciences, and Society, Alzheimer's Disease Research Center, Karolinska Institute, Stockholm, Sweden Department of Psychiatry, Akershus University Hospital, Norway Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway.
Linda R WhiteFaculty of Medicine, Department of Neuroscience, Norwegian University of Science and Technology (NTNU), Trondheim, Norway Department of Neurology, University Hospital of Trondheim, Trondheim, Norway.
Norwegian University of Science and Technology · NOKarolinska Institutet · SEPrivatsykehuset Haugesund · NO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundResults conflict concerning the relevance of APOE alleles on the development of dementia with Lewy bodies (DLB), though they are well established in connection with Alzheimer's disease (AD). The role of APOE alleles in a Norwegian cohort of patients with DLB was therefore examined compared with patients with AD and healthy control individuals.

methodsThe study included 156 patients with DLB diagnosed according to the consensus criteria guidelines, 519 patients diagnosed with AD according to the National Institute of Neurological and Communicative Diseases and Stroke/Alzheimer's Disease and Related Disorders Association (NINCDS/ARDRA) criteria and 643 healthy elderly volunteers. Patients were recruited through hospitals, outpatient clinics, nursing homes or from local care authorities in central and south-western parts of Norway. Healthy individuals were recruited from caregivers and societies for retired people.

resultsSubjects carrying an APOE ε2 allele had a reduced risk for developing DLB (OR 0.4, CI 0.3 to 0.8, p=0.004), and the onset of disease was delayed by 4 years (p=0.01, Mann-Whitney U test). Conversely, the APOE ε4 allele increased the risk for development of DLB (OR 5.9, CI 2.7 to 13.0, p<0.0005 for homozygotes). Similar results were found for patients with AD regarding the effect of APOE ε2, though the protective effect appeared to be slightly less pronounced than in DLB. This study is one of the largest regarding DLB and APOE to date.

conclusionThe results indicate that APOE ε2, a protective factor in AD, has a clear beneficial effect on the development of DLB also.

Indexed as

AgedAge of OnsetAllelesAlzheimer DiseaseApolipoprotein E2Case-Control StudiesFemaleGenotypeHumansLewy Body DiseaseMaleNorwayRisk FactorsApolipoprotein E2Alzheimer's diseaseDementiaGenetics

Identifiers

PMID24639435
PMCPMC4215279
OpenAlexW2114033131

What OpenQuestion holds

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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.