Evidence map›Paper›PMID 25673977›Full record

ArticleClinical interventions in aging2015

Associations between apolipoprotein E gene polymorphisms and Alzheimer's disease risk in a large Chinese Han population.

Ping Wu, Hong-Lei Li, Zhi-Jun Liu, Qing-Qing Tao, Miao Xu, Qi-Hao Guo, Zhen Hong, Yi-Min Sun

Open access · goldAbstract read
In one paragraph

Article in Clinical interventions in aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 2 pooled it
0.9field-weighted citation impact, top 24% 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

6 citing papers in PubMed, 2 syntheses or guidelines pooled it, 16 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Observational
  4. Article
  5. Journal of clinical medicine · 2019
    Article
  6. 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

8 authors at 1 institution in 1 country.

Ping WuDepartment of Neurology and Institute of Neurology, Fudan University, Shanghai, People's Republic of China ; PET Center, Department of Nuclear Medicine, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, People's Republic of China.
Hong-Lei LiDepartment of Neurology and Institute of Neurology, Fudan University, Shanghai, People's Republic of China.
Zhi-Jun LiuDepartment of Neurology and Institute of Neurology, Fudan University, Shanghai, People's Republic of China.
Qing-Qing TaoDepartment of Neurology and Institute of Neurology, Fudan University, Shanghai, People's Republic of China.
Miao XuDepartment of Neurology and Institute of Neurology, Fudan University, Shanghai, People's Republic of China.
Qi-Hao GuoDepartment of Neurology and Institute of Neurology, Fudan University, Shanghai, People's Republic of China.
Zhen HongDepartment of Neurology and Institute of Neurology, Fudan University, Shanghai, People's Republic of China.
Yi-Min SunDepartment of Neurology and Institute of Neurology, Fudan University, Shanghai, People's Republic of China.
Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveApolipoprotein E gene (APOE) polymorphisms contributing to the risk of sporadic Alzheimer's disease (AD) have been identified for decades, but it has not been investigated in large AD samples of Chinese Han population.

methodsWe performed a cross-sectional study to explore the effect of APOE polymorphisms on sporadic AD in 875 sporadic AD patients and 1,195 cognitive normal controls of Chinese Han. Genotyping of APOE was determined by multiplex amplification refractory mutation system polymerase chain reaction.

resultsAPOE ε3ε4 and ε4ε4 genotypes increased AD risk with dosage effect. The odds ratio (OR) of ε3ε4 was 1.89 and the OR of ε4ε4 was 15.64 compared with that of ε3ε3 in all the subjects. E2ε3 genotype decreased AD risk in all the subjects (OR=0.64), female subgroup (OR=0.57), and late-onset AD subgroup (OR=0.60). However, neither ε2ε2 nor ε2ε4 affected AD risk. About the age at onset (AAO), the influence of APOE ε4 was only exhibited in late-onset AD subgroup, with 1 year lower in ε4-positive ones than negative ones. Further analysis did not show the dosage effect of ε4 pertinent to AAO, though the AAO of ε4ε4 patients decreased by 2 years. E2 did not affect the AAO of AD.

conclusionAPOE ε4 is a strong risk factor of AD risk in Chinese Han population, and APOE ε4ε4 genotype might be related to the AAO of late-onset AD.

Indexed as

AgedAged, 80 and overAge of OnsetAllelesAlzheimer DiseaseApolipoprotein E4Asian PeopleChinaCross-Sectional StudiesFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedOdds RatioApolipoprotein E4age at onsetcross sectional studydosage effectsporadic

Identifiers

PMID25673977
PMCPMC4321568
OpenAlexW2075601193

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Registered trials

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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.