Evidence map›Paper›PMID 35888182›Full record

ArticleLife (Basel, Switzerland)2022

Alzheimer's Disease Risk Variant rs3865444 in the

Juraj Javor, Mária Bucová, Vladimíra Ďurmanová, Dominika Radošinská, Zuzana Párnická, Daniel Čierny, Egon Kurča, Daniela Čopíková-Cudráková, Karin Gmitterová, Ivana Shawkatová

Open access · goldAbstract read
In one paragraph

Article in Life (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.7field-weighted citation impact, top 31% 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

2 citing papers in PubMed, 6 citations in OpenAlex.

  1. Review
  2. Review
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

10 authors at 2 institutions in 1 country.

Juraj JavorInstitute of Immunology, Faculty of Medicine, Comenius University in Bratislava, 811 08 Bratislava, Slovakia.ORCID 0000-0002-7741-5779
Mária BucováInstitute of Immunology, Faculty of Medicine, Comenius University in Bratislava, 811 08 Bratislava, Slovakia.
Vladimíra ĎurmanováInstitute of Immunology, Faculty of Medicine, Comenius University in Bratislava, 811 08 Bratislava, Slovakia.
Dominika RadošinskáInstitute of Immunology, Faculty of Medicine, Comenius University in Bratislava, 811 08 Bratislava, Slovakia.
Zuzana PárnickáInstitute of Immunology, Faculty of Medicine, Comenius University in Bratislava, 811 08 Bratislava, Slovakia.
Daniel ČiernyDepartment of Clinical Biochemistry, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava and University Hospital Martin, 036 59 Martin, Slovakia.
Egon KurčaClinic of Neurology, Jessenius Faculty of Medicine in Martin, Comenius University in Bratislava and University Hospital Martin, 036 59 Martin, Slovakia.
Daniela Čopíková-Cudráková1st Department of Neurology, Faculty of Medicine, Comenius University in Bratislava and University Hospital Bratislava, 813 69 Bratislava, Slovakia.
Karin Gmitterová2nd Department of Neurology, Faculty of Medicine, Comenius University in Bratislava and University Hospital Bratislava, 833 05 Bratislava, Slovakia.
Ivana ShawkatováInstitute of Immunology, Faculty of Medicine, Comenius University in Bratislava, 811 08 Bratislava, Slovakia.
Comenius University Bratislava · SKUniversity Hospital Bratislava · SK

Funding

Scientific Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic and the Slovak Academy of Sciences VEGA/1/0738/20
6 · The paper itself

Abstract

Polymorphisms in genes encoding receptors that modulate the activity of microglia and macrophages are attractive candidates for participation in genetic susceptibility to multiple sclerosis (MS). The aims of the study were to (1) investigate the association between Alzheimer’s disease-linked variant rs3865444:C>A in the CD33 gene and MS risk, (2) assess the effect of the strongest MS risk allele HLA-DRB1*15:01 on this association, and (3) analyze the correlation of rs3865444 with selected clinical phenotypes, i.e., age of onset and disease severity. CD33 rs3865444 was genotyped in a cohort of 579 patients and 1145 controls and its association with MS risk and clinical phenotypes was analyzed by logistic and linear regression analysis, respectively. Statistical evaluation revealed that rs3865444 reduces the risk of MS in the HLA-DRB1*15:01-positive subpopulation but not in the cohort negative for HLA-DRB1*15:01. A significant antagonistic epistasis between rs3865444 A and HLA-DRB1*15:01 alleles in the context of MS risk was detected by the interaction synergy factor analysis. Comparison of allele and genotype distribution between relapsing-remitting MS, secondary progressive MS, and control groups revealed that rs3865444 C to A substitution may also be associated with a decreased risk of transition of MS to its secondary progressive form, irrespective of the HLA-DRB1*15:01 carrier status. On the other hand, no correlation could be found between rs3865444 and the age of disease onset or MS severity score. Future studies are required to shed more light on the role of CD33 in MS pathogenesis.

Indexed as

associationCD33multiple sclerosispolymorphismrs3865444severitysusceptibility

Identifiers

PMID35888182
PMCPMC9324428
OpenAlexW4286610797

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.