Evidence map›Paper›PMID 36069947›Full record

ArticleMolecular genetics and genomics : MGG2022

Identification of genetic loci shared between Alzheimer's disease and hypertension.

Megan Sullivan, Hong-Wen Deng, Jonathan Greenbaum

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular genetics and genomics : MGG, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 22% of its field
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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Genome-wide pleiotropy analysis of longitudinal blood pressure and harmonized cognitive performance measures.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
  3. Article
  4. Article
  5. Article
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

3 authors at 1 institution in 1 country.

Megan SullivanTulane Center for Biomedical Informatics and Genomics, School of Medicine, Tulane University, New Orleans, LA, 70112, USA.
Hong-Wen DengTulane Center for Biomedical Informatics and Genomics, School of Medicine, Tulane University, New Orleans, LA, 70112, USA.
Jonathan GreenbaumTulane Center for Biomedical Informatics and Genomics, School of Medicine, Tulane University, New Orleans, LA, 70112, USA. jgreenb8@tulane.edu.ORCID http://orcid.org/0000-0002-7817-5981
Tulane University · US

Funding

Tulane COBRE in Cardiometabolic Diseases Clinical Research CoreP20GM109036 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI Ning Liu · 2016 to 2026
$25.3M
Trans-omics Integration of Multi-omics Studies for OsteoporosisU19AG055373 · NIA · TULANE UNIVERSITY OF LOUISIANA · PI Qi Zhao · 2017 to 2026
$24.3M
Identification of Metabolomic Profiles for Sarcopenia Traits in Older Whites and BlacksR01AG061917 · NIA · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI SHEN, HUI, ZHAO, QI · 2019 to 2023
$3.0M
Decoding Methylation Mediated Epigenomic Contributions to Male OsteoporosisR01AR069055 · NIAMS · TULANE UNIVERSITY OF LOUISIANA · PI DENG, HONG-WEN · 2017 to 2021
$2.9M
NIH HHS P20GM109036NIH HHS R01AG061917NIH HHS R01AR069055NIH HHS U19AG055373
6 · The paper itself

Abstract

Alzheimer's disease (AD) and high blood pressure (BP) are prevalent age-related diseases with significant unexplained heritability. A thorough analysis of genetic pleiotropy between AD and BP will lay a foundation for the study of the associated molecular mechanisms, leading to a better understanding of the development of each phenotype. We used the conditional false discovery rate (cFDR) method to identify novel genetic loci associated with both AD and BP. The cFDR approach improves the effective sample size for association testing by combining GWAS summary statistics for correlated phenotypes. We identified 50 pleiotropic SNPs for AD and BP, 7 of which are novel and have not previously been reported to be associated with either AD or BP. The novel SNPs located at STK3 are particularly noteworthy, as this gene may influence AD risk via the Hippo signaling network, which regulates cell death. Bayesian colocalization analysis demonstrated that although AD and BP are associated, they do not appear to share the same causal variants. We further performed two sample Mendelian randomization analysis, but could not detect a causal effect of BP on AD. Despite the inability to establish a causal link between AD and BP, our findings report some potential novel pleiotropic loci that may influence disease susceptibility. In summary, we identified 7 SNPs that annotate to 4 novel genes which have not previously been reported to be associated with AD nor with BP and discuss the possible role of one of these genes, STK3 in the Hippo signaling network.

Indexed as

Alzheimer DiseaseHypertensionBayes TheoremGenetic LociGenetic Predisposition to DiseaseGenome-Wide Association StudyHippo KinasesHumansPolymorphism, Single NucleotideProtein Serine-Threonine KinasesSerine-Threonine Kinase 3Hippo KinasesProtein Serine-Threonine KinasesSerine-Threonine Kinase 3STK3 protein, humanAlzheimer’s diseaseGWASHypertensionPleiotropy

Identifiers

PMID36069947
OpenAlexW4294919399

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.