Evidence map›Paper›PMID 31055733›Full record

ArticleGeroScience2019

Genetic heterogeneity of Alzheimer's disease in subjects with and without hypertension.

Alireza Nazarian, Konstantin G Arbeev, Arseniy P Yashkin, Alexander M Kulminski

Open access · hybridAbstract readComparative Study
In one paragraph

Article in GeroScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

24 citing papers in PubMed, 32 citations in OpenAlex.

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  17. Non-coding variants in MYH11, FZD3, and SORCS3 are associated with dementia in women.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021
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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

4 authors at 2 institutions in 1 country.

Alireza NazarianBiodemography of Aging Research Unit, Social Science Research Institute, Duke University, Erwin Mill Building, 2024 W. Main St., Durham, NC, 27705, USA. alireza.nazarian@duke.edu.
Konstantin G ArbeevBiodemography of Aging Research Unit, Social Science Research Institute, Duke University, Erwin Mill Building, 2024 W. Main St., Durham, NC, 27705, USA.
Arseniy P YashkinBiodemography of Aging Research Unit, Social Science Research Institute, Duke University, Erwin Mill Building, 2024 W. Main St., Durham, NC, 27705, USA.
Alexander M KulminskiBiodemography of Aging Research Unit, Social Science Research Institute, Duke University, Erwin Mill Building, 2024 W. Main St., Durham, NC, 27705, USA. kulminsk@duke.edu.
Duke University · USSocial Science Research Council · US

Funding

STALLARD Admin Supp: Predicting Future Care Needs and Costs for Individual Medicare Enrollees with Incident Suspected Alzheimer's DiseaseP30AG034424 · NIA · DUKE UNIVERSITY · PI SCOTT M. LYNCH · 2009 to 2026
$12.2M
Relationships among Genetic Regulators of Aging Health and LifespanP01AG043352 · NIA · DUKE UNIVERSITY · PI YASHIN, ANATOLIY I · 2014 to 2018
$8.7M
Molecular signatures of health and life span disparities between whites and African-Americans in the APOE regionR01AG047310 · NIA · DUKE UNIVERSITY · PI KULMINSKI, ALEXANDER M · 2015 to 2019
$2.5M
Explanations of Racial Disparities in Active LifeR03HD050374 · NICHD · PRINCETON UNIVERSITY · PI LYNCH, SCOTT M · 2005 to 2006
$156k
NIA NIH HHS P01 AG043352NIA NIH HHS P01AG043352NIA NIH HHS P30 AG034424NIA NIH HHS R01 AG047310NIA NIH HHS R01AG047310NICHD NIH HHS R03 HD050374
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive neurodegenerative disorder caused by the interplay of multiple genetic and non-genetic factors. Hypertension is one of the AD risk factors that has been linked to underlying pathological changes like senile plaques and neurofibrillary tangles formation as well as hippocampal atrophy. In this study, we investigated the differences in the genetic architecture of AD between hypertensive and non-hypertensive subjects in four independent cohorts. Our genome-wide association analyses revealed significant associations of 15 novel potentially AD-associated polymorphisms (P < 5E-06) that were located outside the chromosome 19q13 region and were significant either in hypertensive or non-hypertensive groups. The closest genes to 14 polymorphisms were not associated with AD at P < 5E-06 in previous genome-wide association studies (GWAS). Also, four of them were located within two chromosomal regions (i.e., 3q13.11 and 17q21.2) that were not associated with AD at P < 5E-06 before. In addition, 30 genes demonstrated evidence of group-specific associations with AD at the false discovery rates (FDR) < 0.05 in our gene-based and transcriptome-wide association analyses. The chromosomal regions corresponding to four genes (i.e., 2p13.1, 9p13.3, 17q12, and 18q21.1) were not associated with AD at P < 5E-06 in previous GWAS. These genes may serve as a list of prioritized candidates for future functional studies. Our pathway-enrichment analyses revealed the associations of 11 non-group-specific and four group-specific pathways with AD at FDR < 0.05. These findings provided novel insights into the potential genetic heterogeneity of AD among subjects with and without hypertension.

Indexed as

Polymorphism, Single NucleotideAgedAged, 80 and overAgingAlzheimer DiseaseCohort StudiesDisease ProgressionFemaleGenetic HeterogeneityGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansHypertensionMalePrognosisProspective StudiesAgingCerebral microvasculatureDementiaGenomicsNeurodegenerative disordersPathway-enrichment analysisTranscriptomics

Identifiers

PMID31055733
PMCPMC6544706
OpenAlexW2943952058

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.