Evidence map›Paper›PMID 34554385›Full record

ArticleGeroScience2022

Mediation of the APOE associations with Alzheimer's and coronary heart diseases through body mass index and lipids.

Yury Loika, Fan Feng, Elena Loiko, Alexander M Kulminski

Open access · greenAbstract read
In one paragraph

Article in GeroScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

12 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Causal mediation analysis of the neuroprotection ofmedRxiv : the preprint server for health sciences · 2025
    Article
  4. SR-B1-/-ApoE-R61h/h Mice Mimic Human Coronary Heart Disease.Cardiovascular drugs and therapy · 2024
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. AD and non-AD mediators of the pathway between the APOE genotype and cognition.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  10. Article
  11. Article
  12. Frontiers in aging neuroscience · 2022
    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

4 authors at 1 institution in 1 country.

Yury LoikaBiodemography of Aging Research Unit, Social Science Research Institute, Duke University, Durham, NC, 27708-0408, USA. yury.loika@duke.edu.ORCID 0000-0001-6730-7320
Fan FengBiodemography of Aging Research Unit, Social Science Research Institute, Duke University, Durham, NC, 27708-0408, USA.
Elena LoikoBiodemography of Aging Research Unit, Social Science Research Institute, Duke University, Durham, NC, 27708-0408, USA.
Alexander M KulminskiBiodemography of Aging Research Unit, Social Science Research Institute, Duke University, Durham, NC, 27708-0408, USA. alexander.kulminski@duke.edu.
Social Science Research Council · US

Funding

Relationships among Genetic Regulators of Aging Health and LifespanP01AG043352 · NIA · DUKE UNIVERSITY · PI YASHIN, ANATOLIY I · 2014 to 2018
$8.7M
ApoE2 and protective molecular signatures in Alzheimer's disease and agingR01AG061853 · NIA · DUKE UNIVERSITY · PI KULMINSKI, ALEXANDER M · 2018 to 2022
$3.9M
Personalized genetic profiles of risk and resilience in Alzheimer's and vascular diseasesR01AG065477 · NIA · DUKE UNIVERSITY · PI KULMINSKI, ALEXANDER M · 2020 to 2024
$3.8M
Dissecting genetic and non-genetic heterogeneity in predisposition to Alzheimer's disease and vascular traits in pleiotropic contextR01AG070488 · NIA · DUKE UNIVERSITY · PI KULMINSKI, ALEXANDER M, OUKRAINTSEVA, SVETLANA V. · 2020 to 2024
$2.8M
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
NIA NIH HHS P01 AG043352NIA NIH HHS R01 AG047310NIA NIH HHS R01 AG061853NIA NIH HHS R01 AG065477NIA NIH HHS R01 AG070488
6 · The paper itself

Abstract

The APOE ε2/ε3/ε4 polymorphism is associated with multiple non-Mendelian traits, including high- (HDL-C) and low- (LDL-C) density lipoprotein cholesterol, triglycerides, body mass index (BMI), coronary heart disease (CHD), and Alzheimer's disease (AD). Lipids and BMI are risk factors for AD and CHD. Causal connections between the ε2 and ε4 alleles and these traits remain, however, poorly understood. We leverage comprehensive analyses of longitudinal data from four studies to examine potentially causal heterogeneous connections between these alleles, lipids, BMI, and diseases. We emphasize mutual mediation roles of lipids and BMI in their associations with the ε2 and ε4 alleles and their mediation roles in the associations of these alleles with AD and CHD. We confirmed previously reported significant univariate associations of these alleles with each trait, except CHD. We found, however, that most of the univariate- and mediation-analysis associations were affected by antagonistic heterogeneity/mediation. The mutual mediation analysis identified the associations of the APOE alleles with LDL-C as the least heterogeneous. The ε2 and ε4 alleles were associated with CHD through lipids, led by beneficial (β

Indexed as

Alzheimer DiseaseApolipoproteins ECoronary DiseaseBody Mass IndexCholesterol, LDLGenotypeHumansTriglyceridesApoE protein, humanApolipoproteins ECholesterol, LDLTriglyceridesAgingAlzheimer’s diseaseApoE polymorphismBody mass indexCoronary heart diseaseHigh-density lipoproteinLow-density lipoproteinTriglycerides

Identifiers

PMID34554385
PMCPMC9135946
OpenAlexW3198991698

What Socratic 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 Socratic graph.