Evidence map›Paper›PMID 39622643›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2025

Transcription Factor-Wide Association Studies to Identify Functional SNPs in Alzheimer's Disease.

Jessica Dunn, Cedric Moore, Nam-Shik Kim, Tianshun Gao, Zhiqiang Cheng, Peng Jin, Guo-Li Ming, Jiang Qian, Yijing Su, Hongjun Song and 1 more

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
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

11 authors.

Jessica DunnDepartment of Pharmacology, Johns Hopkins University, Baltimore, Maryland 21205.ORCID https://orcid.org/0000-0002-3259-9164
Cedric MooreDepartment of Pharmacology, Johns Hopkins University, Baltimore, Maryland 21205.
Nam-Shik KimDepartment of Neuroscience and Mahoney Institute for Neurosciences, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Tianshun GaoDepartment of Ophthalmology, Johns Hopkins University, Baltimore, Maryland 21205.
Zhiqiang ChengDepartment of Pharmacology, Johns Hopkins University, Baltimore, Maryland 21205.
Peng JinDepartment of Human Genetics, Emory University School of Medicine, Atlanta, Georgia 30322.
Guo-Li MingDepartment of Neuroscience and Mahoney Institute for Neurosciences, University of Pennsylvania, Philadelphia, Pennsylvania 19104.
Jiang QianDepartment of Ophthalmology, Johns Hopkins University, Baltimore, Maryland 21205 hzhu4@jhmi.edu shongjun@pennmedicine.upenn.edu yijingsu@upenn.edu qianjiang007@gmail.com.
Yijing SuDepartment of Neuroscience and Mahoney Institute for Neurosciences, University of Pennsylvania, Philadelphia, Pennsylvania 19104 hzhu4@jhmi.edu shongjun@pennmedicine.upenn.edu yijingsu@upenn.edu qianjiang007@gmail.com.
Hongjun SongDepartment of Neuroscience and Mahoney Institute for Neurosciences, University of Pennsylvania, Philadelphia, Pennsylvania 19104 hzhu4@jhmi.edu shongjun@pennmedicine.upenn.edu yijingsu@upenn.edu qianjiang007@gmail.com.
Heng ZhuDepartment of Pharmacology, Johns Hopkins University, Baltimore, Maryland 21205 hzhu4@jhmi.edu shongjun@pennmedicine.upenn.edu yijingsu@upenn.edu qianjiang007@gmail.com.

Funding

Project 4-Early Liver Transplantation for Severe Alcoholic Hepatitis: Animal StudiesP50AA027054 · NIAAA · JOHNS HOPKINS UNIVERSITY · PI ANDREW M. CAMERON · 2019 to 2026
$15.1M
Continuous Neurogenesis in the Mammalian HippocampusR35NS116843 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI HONGJUN SONG · 2020 to 2026
$6.9M
Functional roles of genetic risk factors for brain disorders in neurogenesis and neurodevelopmentR35NS097370 · NINDS · UNIVERSITY OF PENNSYLVANIA · PI MING, GUO-LI · 2017 to 2024
$6.7M
Elucidate the roles of Alzheimer's disease risk genes and variants in gene expression and AD-related phenotypesRF1AG079557 · NIA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GAN, LI, SHEN, YIN · 2022 to 2025
$6.1M
The Chemistry-Biology Interface Program at Johns Hopkins UniversityT32GM080189 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI ROKITA, STEVEN E · 2008 to 2022
$3.5M
High-throughput identification of causal variants underlying neuropsychiatric disease-related GWAS hitsR01MH122451 · NIMH · WASHINGTON UNIVERSITY · PI CORBO, JOSEPH · 2020 to 2024
$3.5M
Proteome-wide analysis of AD-associated SNPsR01AG061852 · NIA · JOHNS HOPKINS UNIVERSITY · PI ZHU, HENG · 2018 to 2022
$2.8M
Connecting AMD SNPs to Functions Using Allele-specific InteractionsR01EY030475 · NEI · JOHNS HOPKINS UNIVERSITY · PI QIAN, JIANG, ZACK, DONALD J. · 2021 to 2025
$2.4M
The Chemistry-Biology Interface Program at Johns Hopkins UniversityT32GM149382 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI STEVEN E ROKITA · 2023 to 2026
$1.4M
NEI NIH HHS R01 EY030475NIAAA NIH HHS P50 AA027054NIA NIH HHS R01 AG061852NIA NIH HHS RF1 AG079557NIGMS NIH HHS T32 GM080189NIGMS NIH HHS T32 GM149382NIMH NIH HHS R01 MH122451NINDS NIH HHS R35 NS097370NINDS NIH HHS R35 NS116843
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder with profound global impact. While genome-wide association studies (GWAS) have revealed genomic variants linked to AD, their translational impact has been limited due to challenges in interpreting the identified genetic associations. To address this challenge, we have devised a novel approach termed transcription factor-wide association studies (TF-WAS). By integrating the GWAS, expression quantitative trait loci, and transcriptome analyses, we selected 30 AD single nucleotide polymorphisms (SNPs) in noncoding regions that are likely to be functional. Using human transcription factor (TF) microarrays, we have identified 90 allele-specific TF interactions with 53 unique TFs. We then focused on several interactions involving SMAD4 and further validated them using electrophoretic mobility shift assay, luciferase, and chromatin immunoprecipitation on engineered genetic backgrounds (female cells). This approach holds promise for unraveling the intricacies of not just AD, but any complex disease with available GWAS data, providing insight into underlying molecular mechanisms and clues toward potential therapeutic targets.

Indexed as

Alzheimer DiseaseGenome-Wide Association StudyPolymorphism, Single NucleotideTranscription FactorsFemaleGenetic Predisposition to DiseaseHumansQuantitative Trait LociSmad4 ProteinSmad4 ProteinSMAD4 protein, humanTranscription FactorsAlzheimer’s diseaseSNPsTF-WAS

Identifiers

PMID39622643
PMCPMC11714347

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.