Evidence map›Paper›PMID 37700353›Full record

SynthesisActa neuropathologica communications2023

APOE-ε4 and BIN1 increase risk of Alzheimer's disease pathology but not specifically of Lewy body pathology.

Seth Talyansky, Yann Le Guen, Nandita Kasireddy, Michael E Belloy, Michael D Greicius

Abstract readMeta-Analysis
In one paragraph

Synthesis in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. TMEM106B is a selective modulator of TDP-43 pathology in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Shared genetic architecture between DTI-ALPS traits and neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  5. Review
  6. Effects of α-synuclein pathology on synaptic dysfunction and clinical outcomes in normal aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  7. Review
  8. Celebrating neuropathology's contributions to Alzheimer's Disease Research Centers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  9. 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
  10. Article
  11. Review
  12. Article
  13. Multifaceted roles of APOE in Alzheimer disease.Nature reviews. Neurology · 2024
    Review
  14. Apolipoprotein E Gene in α-Synucleinopathies: A Narrative Review.International journal of molecular sciences · 2024
    Review
  15. Review
  16. Article
4 · The record

Corrections and comments

  • Update of
    2023
5 · Who and what money

Authors and funding

5 authors.

Seth Talyansky *Department of Neurology and Neurological Sciences, Stanford University, 290 Jane Stanford Way, E265, Stanford, CA, 94305-5090, USA.
Yann Le Guen *Department of Neurology and Neurological Sciences, Stanford University, 290 Jane Stanford Way, E265, Stanford, CA, 94305-5090, USA. yleguen@stanford.edu.ORCID http://orcid.org/0000-0001-6649-8364
Nandita KasireddyDepartment of Neurology and Neurological Sciences, Stanford University, 290 Jane Stanford Way, E265, Stanford, CA, 94305-5090, USA.
Michael E BelloyDepartment of Neurology and Neurological Sciences, Stanford University, 290 Jane Stanford Way, E265, Stanford, CA, 94305-5090, USA.
Michael D GreiciusDepartment of Neurology and Neurological Sciences, Stanford University, 290 Jane Stanford Way, E265, Stanford, CA, 94305-5090, USA.

Funding

The Stanford Extreme Phenotypes in Alzheimer's Disease (StEP AD) CohortR01AG060747 · NIA · STANFORD UNIVERSITY · PI GREICIUS, MICHAEL D · 2018 to 2022
$3.4M
Elucidating sex-specific risk for Alzheimer's disease through state-of-the-art genetics and multi-omicsK99AG075238 · NIA · STANFORD UNIVERSITY · PI BELLOY, MICHAEL · 2022 to 2023
$264k
NIA NIH HHS K99 AG075238NIA NIH HHS R01 AG060747
6 · The paper itself

Abstract

Lewy body (LB) pathology commonly occurs in individuals with Alzheimer's disease (AD) pathology. However, it remains unclear which genetic risk factors underlie AD pathology, LB pathology, or AD-LB co-pathology. Notably, whether APOE-ε4 affects risk of LB pathology independently from AD pathology is controversial. We adapted criteria from the literature to classify 4,985 subjects from the National Alzheimer's Coordinating Center (NACC) and the Rush University Medical Center as AD-LB co-pathology (AD

Indexed as

Alzheimer DiseaseAdaptor Proteins, Signal TransducingApolipoproteins EGenome-Wide Association StudyHumansLewy BodiesNeuropathologyNuclear ProteinsTumor Suppressor ProteinsAdaptor Proteins, Signal TransducingApoE protein, humanApolipoproteins EBIN1 protein, humanNuclear ProteinsTumor Suppressor ProteinsAlzheimer’s disease pathologyAPOE-ε4BIN1Co-pathologyGenetic riskGWASLewy body pathology

Identifiers

PMID37700353
PMCPMC10496176

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.