Evidence map›Paper›PMID 41966729›Full record

ArticleEBioMedicine2026

Distinct metabolic signatures of Alzheimer's and Parkinson's disease revealed through genetic overlap.

Sara E Stinson, Alexey A Shadrin, Zillur Rahman, Linn Rødevand, Iris J Broce, Geir Selbæk, Hreinn Stefansson, Jan Haavik, Nadine Parker, Elise Koch and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–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

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Sara E StinsonCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway. Electronic address: sstins@ous-hf.no.
Alexey A ShadrinCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway; K.G. Jebsen Centre for Neurodevelopmental Disorders, University of Oslo and Oslo University Hospital, Oslo, Norway.
Zillur RahmanCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Linn RødevandCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Iris J BroceCenter for Multimodal Imaging and Genetics, J. Craig Venter Institute, La Jolla, CA, USA; University of California San Diego, La Jolla, CA, USA.
Geir SelbækDepartment of Geriatric Medicine, Oslo University Hospital, Oslo, Norway; The Norwegian National Centre for Ageing and Health, Vestfold Hospital Trust, Tønsberg, Norway.
Hreinn StefanssonAMGEN deCODE Genetics, Reykjavik, Iceland.
Jan HaavikDepartment of Biomedicine, Faculty of Medicine, University of Bergen, Bergen, Norway; Division of Psychiatry, Haukeland University Hospital, Bergen, Norway.
Nadine ParkerCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Elise KochCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Oleksandr FreiCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Kevin S O'ConnellCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Olav B SmelandCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Srdjan DjurovicCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Medical Genetics, Oslo University Hospital & University of Oslo, Oslo, Norway.
Anders M DaleCenter for Multimodal Imaging and Genetics, J. Craig Venter Institute, La Jolla, CA, USA; University of California San Diego, La Jolla, CA, USA.
Dennis van der MeerCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Ole A AndreassenCentre for Precision Psychiatry, Division of Mental Health and Addiction, Oslo University Hospital & Institute of Clinical Medicine, University of Oslo, Oslo, Norway; K.G. Jebsen Centre for Neurodevelopmental Disorders, University of Oslo and Oslo University Hospital, Oslo, Norway. Electronic address: ole.andreassen@medisin.uio.no.

Funding

Novel imaging genetic biomarkers for sporadic frontotemporal dementia through machine learningK01AG070376 · UNIVERSITY OF CALIFORNIA, SAN DIEGO · 2025 to 2025
$83k
NIA NIH HHS K01 AG070376
6 · The paper itself

Abstract

backgroundMetabolic dysfunction is a major risk factor for neurodegeneration, yet the genetic architecture linking systemic metabolism to Alzheimer's disease (AD) and Parkinson's disease (PD) remains unclear.

methodsWe integrated genome-wide association data for 249 circulating metabolites and proglucagon with summary statistics for AD, PD, and cardiometabolic traits. Genetic correlations, polygenic overlap, causal relationships, and shared genetic loci were quantified using linkage disequilibrium score regression, high-definition likelihood, bivariate mixture modelling, Mendelian randomisation, and conjunctional false discovery rate analyses, followed by functional and tissue-specific enrichment analyses.

findingsAD displayed a metabolic-genetic profile aligned with body mass index, type 2 diabetes, coronary artery disease, and stroke, whereas PD exhibited largely opposing patterns (Spearman's r

interpretationAD and PD are shaped by fundamentally distinct metabolic-genetic architectures. Metabolically targeted interventions, particularly those modulating lipid, amino acid, and proglucagon pathways, may require disease-specific and genetically informed strategies for prevention and treatment of neurodegenerative diseases.

fundingNovo Nordisk Foundation (NNF23OC0099658), Marie Skłodowska-Curie Actions (801133), the Research Council of Norway (334920, 351751, 296030, 324252, 324499, 326813), the National Institutes of Health (U24DA041123, R01AG076838, U24DA055330, OT2HL161847, 5R01MH124839-02), NordForsk (164218), South-Eastern Norway Regional Health Authority (2020060), and the European Union's Horizon 2020 (847776, 964874, 101057454).

Indexed as

Alzheimer DiseaseMetabolomeParkinson DiseaseGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLinkage DisequilibriumMendelian Randomization AnalysisMetabolomicsPolymorphism, Single NucleotideAlzheimer's diseaseCardiometabolic diseaseGenome-wide association studyMetabolomicsParkinson's diseaseProglucagon

Identifiers

PMID41966729
PMCPMC13091360

What Socratic 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 Socratic graph.