Evidence map›Paper›PMID 25204495›Full record

ArticleMolecular neurobiology2015

Integrating Genome-Wide Association Study and Brain Expression Data Highlights Cell Adhesion Molecules and Purine Metabolism in Alzheimer's Disease.

Zimin Xiang, Meiling Xu, Mingzhi Liao, Yongshuai Jiang, Qinghua Jiang, Rennan Feng, Liangcai Zhang, Guoda Ma, Guangyu Wang, Zugen Chen and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 4 pooled it
2.1field-weighted citation impact, top 14% 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

23 citing papers in PubMed, 4 syntheses or guidelines pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Rs4878104 contributes to Alzheimer's disease risk and regulates DAPK1 gene expression.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017
    Article
  20. 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

14 authors at 10 institutions in 2 countries.

Zimin XiangDepartment of Orthopedic Surgery, Beijing Army General Hospital, Clinical Medicine College of Third Military Medical University, No. 5 Nanmencang, Dongcheng District, Beijing, 100700, China.
Meiling Xu
Mingzhi Liao
Yongshuai Jiang
Qinghua Jiang
Rennan Feng
Liangcai Zhang
Guoda Ma
Guangyu Wang
Zugen Chen
Bin Zhao
Tiansheng Sun
Keshen Li
Guiyou Liu
Guangdong Medical College · CNHarbin Medical University · CNThe Military General Hospital of Beijing PLA · CNChinese Academy of Sciences · CNFirst Affiliated Hospital of Harbin Medical University · CNFourth Affiliated Hospital of Harbin Medical University · CNHarbin Institute of Technology · CNNorthwest A&F University · CNRice University · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common neurodegenerative disease in the elderly. Recently, genome-wide association studies (GWAS) have been used to investigate AD pathogenesis. However, a large proportion of AD heritability has yet to be explained. We previously identified the cell adhesion molecule (CAM) pathway as a consistent signal in two AD GWAS. However, it is unclear whether CAM is present in the Genetic and Environmental Risk for Alzheimer's Disease Consortium (GERAD) GWAS and brain expression GWAS. Meanwhile, we think integrating AD GWAS and AD brain expression datasets may provide complementary information to identify important pathways involved in AD. Here, we conducted a systems analysis using (1) KEGG pathways, (2) large-scale AD GWAS from GERAD (n = 11,789), (3) two brain expression GWAS datasets (n = 399) from the AD cerebellum and temporal cortex, and (4) previous results from pathway analysis of AD GWAS. Our results indicate that (1) CAM is a consistent signal in five AD GWAS; (2) CAM is the most significant signal in AD; (3) we confirmed previous AD risk pathways related to immune system and diseases, and cardiovascular disease, etc.; and (4) we highlighted the purine metabolism pathway in AD for the first time. We believe that our results may advance our understanding of AD mechanisms and will be very informative for future genetic studies in AD.

Indexed as

Gene Expression RegulationGenome-Wide Association StudyAlzheimer DiseaseBrainCell Adhesion MoleculesDatabases, GeneticGenetic Predisposition to DiseaseHumansMetabolic Networks and PathwaysPurinesRisk FactorsCell Adhesion MoleculesPurines

Identifiers

PMID25204495
OpenAlexW1967145306

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.