Evidence map›Paper›PMID 26795201›Full record

SynthesisMedical science monitor : international medical journal of experimental and clinical research2016

Associations Between Genetic Variants in 19p13 and 19q13 Regions and Susceptibility to Alzheimer Disease: A Meta-Analysis.

Jie Bao, Xiao-jie Wang, Zong-fu Mao

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Medical science monitor : international medical journal of experimental and clinical research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 3 pooled it
1.9field-weighted citation impact, top 13% 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

15 citing papers in PubMed, 3 syntheses or guidelines pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Article
  6. Heterogeneity in Alzheimer's Disease Diagnosis and Progression Rates: Implications for Therapeutic Trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Review
  7. Article
  8. Article
  9. Article
  10. CSF and blood Kallikrein-8: a promising early biomarker for Alzheimer's disease.Journal of neurology, neurosurgery, and psychiatry · 2020
    Article
  11. Article
  12. Article
  13. Article
  14. A Novel Method to Identify Differential Pathways in Hippocampus Alzheimer's Disease.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Article
  15. Reply to Liu and Jiang: Maintenance of postreproductive cognitive capacity by inclusive fitness.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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 2 institutions in 1 country.

Jie BaoGlobal Health Institute, Wuhan University, Wuhan, Hubei, China (mainland).
Xiao-jie WangWuhan Women and Children Medical Care Center, Wuhan, Hubei, China (mainland).
Zong-fu MaoGlobal Health Institute, Wuhan University, Wuhan, Hubei, China (mainland).
Wuhan University · CNWuhan Medical Center for Women and Children · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlzheimer disease (AD) has become an epidemic within the growing elderly population and effective therapies of AD have not been discovered. Genetic factors accounted for over 70% of the incidence of AD and the disease-related polymorphisms are located on chromosome 19, which is one of several prominent chromosomes related to the development of AD. Many inconsistent associations between polymorphisms in ABCA7, CD33, and TOMM40 genes and the susceptibility to AD have been suggested by several independent studies. MATERIAL/

methodsA comprehensive literature search for studies involving the association between gene polymorphisms and AD was performed, and we finally selected 3 genes (4 polymorphisms) for the meta-analysis: ABCA7 (rs3764650), CD33 (rs3865444), and TOMM40 (rs157580, rs2075650).

resultsA total of 25 articles investigating 3 genes (4 polymorphisms) were included in the meta-analysis. The pooled results of 4 polymorphisms were all significantly associated with the susceptibility to AD. The pooled effect of ABCA7 rs3764605 allele G was significantly associated with an increased the risk of AD (OR=1.20, 95% CI: 1.14-1.26, P value <0.001). Similarly, our evidence suggested that allele A of TOMM40 rs2075650 polymorphism was a risk factor for AD (OR=2.87, 95% CI: 2.46-3.34, P value <0.001). Alleles A of CD33 rs3865444 and A of TOMM40 rs157580 were both protective factors for AD onset (OR=0.94, 95% CI: 0.90-0.98, P value=0.003; OR=0.62, 95% CI: 0.57-0.66, P value <0.001). CONCLUSIONS" Results from the meta-analysis revealed that the pooled ABCA7 rs376465, CD33 rs3865444, TOMM40 rs157580, and rs2075650 variants were significantly associated with the susceptibility to AD. However, the association differed significantly between Asian and Caucasian groups for SNPs of CD33 rs3865444, TOMM40 rs157580, and rs2075650.

Indexed as

Genetic Association StudiesGenetic Predisposition to DiseaseGenetic VariationAlzheimer DiseaseATP-Binding Cassette TransportersChromosomes, Human, Pair 19HumansMembrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsMutationPublication BiasSialic Acid Binding Ig-like Lectin 3ABCA7 protein, humanATP-Binding Cassette TransportersCD33 protein, humanMembrane Transport ProteinsMitochondrial Precursor Protein Import Complex ProteinsSialic Acid Binding Ig-like Lectin 3TOMM40 protein, human

Identifiers

PMID26795201
PMCPMC4727495
OpenAlexW2292600671

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.