Evidence map›Paper›PMID 26746668›Full record

ArticleMolecular neurobiology2017

Alzheimer's Disease Variants with the Genome-Wide Significance are Significantly Enriched in Immune Pathways and Active in Immune Cells.

Qinghua Jiang, Shuilin Jin, Yongshuai Jiang, Mingzhi Liao, Rennan Feng, Liangcai Zhang, Guiyou Liu, Junwei Hao

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Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 6 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 6 pooled it
–field-weighted citation impact
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

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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

71 citing papers in PubMed, 6 syntheses or guidelines pooled it.

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  12. Acquired immunity and Alzheimer's disease.Journal of biomedical research · 2022
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11 more citing papers are in PubMed but not listed here.

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.

Qinghua JiangSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China.
Shuilin JinDepartment of Mathematics, Harbin Institute of Technology, Harbin, China.
Yongshuai JiangCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Mingzhi LiaoCollege of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
Rennan FengDepartment of Nutrition and Food Hygiene, School of Public Health, Harbin Medical University, Harbin, China.
Liangcai ZhangDepartment of Statistics, Rice University, Houston, TX, USA.
Guiyou LiuSchool of Life Science and Technology, Harbin Institute of Technology, Harbin, China. liuguiyou1981@163.com.
Junwei HaoDepartment of Neurology and Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The existing large-scale genome-wide association studies (GWAS) datasets provide strong support for investigating the mechanisms of Alzheimer's disease (AD) by applying multiple methods of pathway analysis. Previous studies using selected single nucleotide polymorphisms (SNPs) with several thresholds of nominal significance for pathway analysis determined that the threshold chosen for SNPs can reflect the disease model. Presumably, then, pathway analysis with a stringent threshold to define "associated" SNPs would test the hypothesis that highly associated SNPs are enriched in one or more particular pathways. Here, we selected 599 AD variants (P < 5.00E-08) to investigate the pathways in which these variants are enriched and the cell types in which these variants are active. Our results showed that AD variants are significantly enriched in pathways of the immune system. Further analysis indicated that AD variants are significantly enriched for enhancers in a number of cell types, in particular the B-lymphocyte, which is the most substantially enriched cell type. This cell type maintains its dominance among the strongest enhancers. AD SNPs also display significant enrichment for DNase in 12 cell types, among which the top 6 significant signals are from immune cell types, including 4 B cells (top 4 significant signals) and CD14+ and CD34+ cells. In summary, our results show that these AD variants with P < 5.00E-08 are significantly enriched in pathways of the immune system and active in immune cells. To a certain degree, the genetic predisposition for development of AD is rooted in the immune system, rather than in neuronal cells.

Indexed as

Alzheimer DiseaseDatabases, GeneticGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansImmune System DiseasesImmunity, CellularAlzheimer’s diseaseGenome-wide association studyImmune cellsImmune pathwaysPathway analysis

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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.