Evidence map›Paper›PMID 42566020›Full record

ArticleEuropean journal of nuclear medicine and molecular imaging2026

Effect of genetic factors on [

Sofie Lövdal, Sanne K Meles, Giulia Carli, Anna Dortmond, Rosalie V Kogan, Orly Goldstein, Mali Gana-Weisz, Rotem I Orad, Roy N Alcalay, Noa Bregman and 2 more

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Article in European journal of nuclear medicine and molecular imaging, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

12 authors.

Sofie LövdalDepartment of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Sanne K MelesDepartment of Neurology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Giulia CarliMorris K. Udall Center of Excellence for Parkinson's Disease Research, University of Michigan, Ann Arbor, MI, USA.
Anna DortmondDepartment of Neurology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Rosalie V KoganDepartment of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Orly GoldsteinLaboratory of Biomarkers and Genomics of Neurodegeneration. Tel-Aviv Medical Center, Tel-Aviv, Israel.
Mali Gana-WeiszLaboratory of Biomarkers and Genomics of Neurodegeneration. Tel-Aviv Medical Center, Tel-Aviv, Israel.
Rotem I OradGray Faculty of Medical & Health Sciences, Tel-Aviv University, Tel-Aviv, Israel.
Roy N AlcalayGray Faculty of Medical & Health Sciences, Tel-Aviv University, Tel-Aviv, Israel.
Noa BregmanGray Faculty of Medical & Health Sciences, Tel-Aviv University, Tel-Aviv, Israel.
Klaus L LeendersDepartment of Nuclear Medicine and Molecular Imaging, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
Tamara ShinerGray Faculty of Medical & Health Sciences, Tel-Aviv University, Tel-Aviv, Israel. tamarashiner@gmail.com.ORCID http://orcid.org/0000-0002-6368-9656

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroimaging with [

objectivesTo determine whether GBA1 and APOE ε4 status are associated with diverging [

methodsWe analyzed [

resultsAPOE ε4 status mainly influenced the CIS, with APOE ε4-negative patients showing greater preservation of the DLB-typical CIS pattern (p = 0.03) compared to APOE ε4 carriers. In contrast, GBA1 status influenced global metabolic phenotype. GBA1 carriers showed a more homogeneous PD/DLB-like metabolic pattern in the machine learning model (p = 0.003) compared to GBA1 non-carriers, whereas the latter group demonstrated greater heterogeneity and higher expression of the AD-related metabolic pattern (p = 0.004). These effects were observed along a metabolic spectrum rather than as distinct clusters.

conclusionsAPOE ε4 and GBA1 modulate distinct aspects of the metabolic phenotype in DLB. GBA1 non-carriers and APOE ε4 carriers showed a higher rate of atypical metabolic signatures, which may contribute to biological heterogeneity and increase the risk of diagnostic misclassification.

Indexed as

[18F]FDG PETAPOE polymorphismsDementia with Lewy BodiesGBA mutations

Identifiers

What OpenQuestion holds

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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.