Evidence map›Paper›PMID 30319691›Full record

ArticleFrontiers in genetics2018

Genome-Wide Association and Mechanistic Studies Indicate That Immune Response Contributes to Alzheimer's Disease Development.

Changan Liu, Jacqueline Chyr, Weiling Zhao, Yungang Xu, Zhiwei Ji, Hua Tan, Claudio Soto, Xiaobo Zhou, Alzheimer’s Disease Neuroimaging Initiative

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 55 citations in OpenAlex.

  1. Pooled it
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  16. Privacy protection of medical data in social network.BMC medical informatics and decision making · 2021
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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 1 institution in 1 country.

Changan LiuSchool of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Jacqueline ChyrSchool of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Weiling ZhaoSchool of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Yungang XuSchool of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Zhiwei JiSchool of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Hua TanSchool of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Claudio SotoDepartment of Neurology, The George and Cynthia W Mitchell Center for Alzheimer's Disease and Other Brain Related Illnesses, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Xiaobo ZhouSchool of Biomedical Informatics, The University of Texas Health Science Center at Houston, Houston, TX, United States.
Alzheimer’s Disease Neuroimaging Initiative
The University of Texas Health Science Center at Houston · US

Funding

Alzheimer's Disease Neuroimaging Initiative - SupplementU01AG024904 · NIA · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI WEINER, MICHAEL W · 2004 to 2015
$121.0M
NIA NIH HHS U01 AG024904
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the most common cause of dementia. Although genome-wide association study (GWAS) have reported hundreds of single-nucleotide polymorphisms (SNPs) and genes linked to AD, the mechanisms about how these SNPs modulate the development of AD remain largely unknown. In this study, we performed GWAS for three traits in cerebrospinal fluid (CSF) and one clinical trait in the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. Our analysis identified five most significant AD related SNPs (FDR < 0.05) within or proximal to APOE, APOC1, and TOMM40. One of the SNPs was co-inherited with APOE allele 4, which is the most important genetic risk factor for AD. Three of the five SNPs were located in promoter or enhancer regions, and transcription factor (TF) binding affinity calculations showed dramatic changes (| Log2FC| > 2) of three TFs (PLAG1, RREB1, and ZBTB33) for two motifs containing SNPs rs2075650 and rs157580. In addition, our GWAS showed that both rs2075650 and rs157580 were significantly associated with the poliovirus receptor-related 2 (PVRL2) gene (FDR < 0.25), which is involved in spreading of herpes simplex virus (HSV). The altered regulation of PVRL2 may increase the susceptibility AD patients to HSV and other virus infections of the brain. Our work suggests that AD is a type of immune disorder driven by viral or microbial infections of the brain during aging.

Indexed as

Alzheimer’s diseasebinding affinityGWASimmune disordersmechanismregulationSNPtranscription factor

Identifiers

PMID30319691
PMCPMC6166008
OpenAlexW2893415830

What OpenQuestion holds

Textmetadata
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.