Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
0numbers the graph read from it
0cells of the map it votes in
3citing 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.
Arvis SulovariCajal Neuroscience, Seattle, WA, USA.
Samuel N SmukowskiDivision of Medical Genetics, University of Washington School of Medicine, Seattle, WA, USA.
Yidian YeDivision of Medical Genetics, University of Washington School of Medicine, Seattle, WA, USA.
Ian PeikonCajal Neuroscience, Seattle, WA, USA.
Suman JayadevDivision of Medical Genetics, University of Washington School of Medicine, Seattle, WA, USA.ORCID 0000-0003-3164-9665
Benjamin A LogsdonCajal Neuroscience, Seattle, WA, USA.
Ellen M WijsmanDivision of Medical Genetics, University of Washington School of Medicine, Seattle, WA, USA.ORCID 0000-0002-2725-6669
Elizabeth E BlueDivision of Medical Genetics, University of Washington School of Medicine, Seattle, WA, USA.ORCID 0000-0002-0633-0305
Paul N ValdmanisDivision of Medical Genetics, University of Washington School of Medicine, Seattle, WA, USA. paulnv@uw.edu.ORCID 0000-0001-8840-6969
Funding
University of Washington Alzheimer's Disease Research CenterP30AG066509 · NIA · UNIVERSITY OF WASHINGTON · PI Amanda D. Boyd · 2020 to 2026
$29.0M
Therapeutic target discovery in ADSP data via comprehensive whole-genome analysis incorporating ethnic diversity and systems approachesU01AG058589 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BOERWINKLE, ERIC A., DE JAGER, PHILIP L · 2018 to 2022
$11.1M
Novel approaches to identify tandem repeat expansions in neurodegenerative diseaseR01NS122766 · NINDS · UNIVERSITY OF WASHINGTON · PI Paul Nils Valdmanis · 2022 to 2026
$1.9M
Interrogating the protective effect of African APOE alleles on Alzheimer's disease risk through pleiotropyR21AG089267 · NIA · UNIVERSITY OF WASHINGTON · PI BLUE, ELIZABETH ELOYCE · 2024 to 2025
$428k
Leveraging PSEN2 biology to understand 3’UTR regulation in Alzheimer’s diseaseK00NS125830 · NINDS · UNIVERSITY OF WASHINGTON · PI Julianna Nicole Dunbar · 2023 to 2026
$328k
NIA NIH HHS P30 AG066509NINDS NIH HHS K00 NS125830U.S. Department of Health & Human Services | National Institutes of Health (NIH) K00NS125830U.S. Department of Health & Human Services | National Institutes of Health (NIH) R21AG089267U.S. Department of Health & Human Services | National Institutes of Health (NIH) U01AG058589U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) R01NS122766
6 · The paper itself
Abstract
The APOE-ε4/ε4 genotype is the strongest genetic risk factor for sporadic Alzheimer's disease, though the relative risk is diminished in individuals with African ancestry. Through analysis of phased APOE alleles, we identify a 19 bp deletion approximately 1.1 kb distal to the APOE 3'UTR in a SPI1 microglial transcription factor binding site. The deletion is present in 60% of African American APOE-ε4 homozygotes and reduces Alzheimer's disease odds ratio relative to individuals without the deletion. The deletion also delays Alzheimer's disease onset in APOE-ε4/ε4 cases with local African ancestry at APOE. The All of Us dataset confirms reduced Alzheimer´s disease risk associated with the deletion and identifies additional variants between APOE and APOC1 that disentangle APOE-ε4 neurological and lipid-related phenotypes. Functional assays reveal that the 19 bp deletion abolishes SPI1 repression at this region. Collectively, these findings describe a protective allele at APOE in African Americans that mediates APOC1 expression, reducing relative Alzheimer´s disease risk.
Indexed as
Alzheimer DiseaseApolipoprotein E4Apolipoproteins EBlack or African AmericanEnhancer Elements, GeneticSequence Deletion3' Untranslated RegionsAgedAllelesApolipoprotein C-IFemaleGenetic Predisposition to DiseaseGenotypeHumansMale3' Untranslated RegionsAPOC1 protein, humanApolipoprotein C-IApolipoprotein E4Apolipoproteins E
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.
A common 19 bp APOE enhancer deletion is protective against Alzheimer's disease in African Americans. · full record | OpenQuestion