Evidence map›Paper›PMID 34155245›Full record

ArticleScientific reports2021

Interaction between genetic predisposition, smoking, and dementia risk: a population-based cohort study.

Na Zhang, Janice M Ranson, Zhi-Jie Zheng, Eilis Hannon, Zhenwei Zhou, Xuejun Kong, David J Llewellyn, Daniel A King, Jie Huang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.

  1. Pooled it
  2. Smoking Interacts WithBiological psychiatry global open science · 2026
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  5. Review
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  12. Article
  13. Socioeconomic Deprivation, Genetic Risk, and Incident Dementia.American journal of preventive medicine · 2023
    Article
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  15. Article
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  18. 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

9 authors at 5 institutions in 3 countries.

Na ZhangDepartment of Global Health, Peking University School of Public Health, Beijing, China.
Janice M RansonCollege of Medicine and Health, University of Exeter, Exeter, UK.
Zhi-Jie ZhengDepartment of Global Health, Peking University School of Public Health, Beijing, China.
Eilis HannonCollege of Medicine and Health, University of Exeter, Exeter, UK.
Zhenwei ZhouDepartment of Biostatistics, Boston University, Boston, MA, USA.
Xuejun KongDepartment of Psychiatry, Beth Israel Deaconess Medical Center, Boston, MA, USA.
David J LlewellynCollege of Medicine and Health, University of Exeter, Exeter, UK.
Daniel A KingDepartment of Medicine, Stanford University School of Medicine, Stanford, CA, USA.
Jie HuangDepartment of Global Health, Peking University School of Public Health, Beijing, China. jiehuang001@pku.edu.cn.ORCID 0000-0002-9036-4304
Peking University · CNUniversity of Exeter · GBBeth Israel Deaconess Medical Center · USBoston University · USStanford University · US

Funding

Identifying modifiable aspects of gene-by-environment interplay in later-life cognitive declineRF1AG055654 · NIA · UNIVERSITY OF SOUTHERN CALIFORNIA · PI FAUL, JESSICA, GALAMA, TITUS JOHANNES · 2017 to 2018
$4.3M
Medical Research Council MC_PC_17228Medical Research Council MC_QA137853NIA NIH HHS RF1 AG055654
6 · The paper itself

Abstract

We evaluated whether the association between cigarette smoking and dementia risk is modified by genetic predisposition including apolipoprotein E (APOE) genotype and polygenic risk (excluding the APOE region). We included 193,198 UK Biobank participants aged 60-73 years without dementia at baseline. Of non-APOE-ε4 carriers, 0.89% (95% CI 0.73-1.08%) current smokers developed dementia compared with 0.49% (95% CI 0.44-0.55%) of never smokers (adjusted HR 1.78; 95% CI 1.39-2.29). In contrast, of one APOE-ε4 allele carriers, 1.69% (95% CI 1.31-2.12%) current smokers developed dementia compared with 1.40% (95% CI 1.25-1.55%) of never smokers (adjusted HR 1.06; 95% CI 0.77-1.45); of two APOE-ε4 alleles carriers, 4.90% (95% CI 2.92-7.61%) current smokers developed dementia compared with 3.87% (95% CI 3.11-4.74%) of never smokers (adjusted HR 0.94; 95% CI 0.49-1.79). Of participants with high polygenic risk, 1.77% (95% CI 1.35-2.27%) current smokers developed dementia compared with 1.05% (95% CI 0.91-1.21%) of never smokers (adjusted HR 1.63; 95% CI 1.16-2.28). A significant interaction was found between APOE genotype and smoking status (P = 0.002) while no significant interaction was identified between polygenic risk and smoking status (P = 0.25). APOE genotype but not polygenic risk modified the effect of smoking on dementia risk.

Indexed as

Disease SusceptibilityGenetic Predisposition to DiseaseAdultAgedAllelesDementiaFemaleGenotypeHumansMaleMiddle AgedPolymorphism, Single NucleotidePopulation SurveillanceRisk AssessmentRisk FactorsSmoking

Identifiers

PMID34155245
PMCPMC8217565
OpenAlexW3135706667

What OpenQuestion holds

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LicenceCC BY
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.