Evidence map›Paper›PMID 34291080›Full record

ArticleFrontiers in molecular biosciences2021

GWAS-Top Polymorphisms Associated With Late-Onset Alzheimer Disease in Brazil: Pointing Out Possible New Culprits Among Non-Coding RNAs.

Gabriela Canalli Kretzschmar, Nina Moura Alencar, Saritha Suellen Lopes da Silva, Carla Daniela Sulzbach, Caroline Grisbach Meissner, Maria Luiza Petzl-Erler, Ricardo Lehtonen R Souza, Angelica Beate Winter Boldt

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular biosciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. MissingGenes · 2021
    Review
  6. 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

8 authors at 1 institution in 1 country.

Gabriela Canalli KretzschmarLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Nina Moura AlencarLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Saritha Suellen Lopes da SilvaLaboratory of Polymorphism and Linkage, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Carla Daniela SulzbachLaboratory of Polymorphism and Linkage, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Caroline Grisbach MeissnerLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Maria Luiza Petzl-ErlerLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Ricardo Lehtonen R SouzaLaboratory of Polymorphism and Linkage, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Angelica Beate Winter BoldtLaboratory of Human Molecular Genetics, Postgraduate Program in Genetics, Department of Genetics, Federal University of Paraná, Curitiba, Brazil.
Universidade Federal do Paraná · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several genome-wide association studies (GWAS) have been carried out with late-onset Alzheimer's disease (LOAD), mainly in European and Asian populations. Different polymorphisms were associated, but several of them without a functional explanation. GWAS are fundamental for identifying loci associated with diseases, although they often do not point to causal polymorphisms. In this sense, functional investigations are a fundamental tool for discovering causality, although the failure of this validation does not necessarily indicate a non-causality. Furthermore, the allele frequency of associated genetic variants may vary widely between populations, requiring replication of these associations in other ethnicities. In this sense, our study sought to replicate in 150 AD patients and 114 elderly controls from the South Brazilian population 18 single-nucleotide polymorphisms (SNPs) associated with AD in European GWAS, with further functional investigation using bioinformatic tools for the associated SNPs. Of the 18 SNPs investigated, only four were associated in our population: rs769449 (

Indexed as

Alzheimer’s diseaseAPOEBIN1CELF1GWASlncRNAmiRNA

Identifiers

PMID34291080
PMCPMC8287568
OpenAlexW3186840833

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.