Evidence map›Paper›PMID 28745649›Full record

ArticleJournal of visualized experiments : JoVE2017

High-resolution Melting PCR for Complement Receptor 1 Length Polymorphism Genotyping: An Innovative Tool for Alzheimer's Disease Gene Susceptibility Assessment.

Aymric Kisserli, Thierry Tabary, Jacques Henri Max Cohen, Valérie Duret, Rachid Mahmoudi

Registry-linked trialAbstract read
In one paragraph

Article in Journal of visualized experiments : JoVE, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02770482 (Utility of Amyloid Beta-peptide 1-40 Measurement in the Diagnosis of Alzheimer's Disease), which is not on this 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
–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

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.

NCT02770482 nacompletednot on this map

Utility of Amyloid Beta-peptide 1-40 Measurement in the Diagnosis of Alzheimer's Disease

TypeinterventionalSponsorCHU de ReimsRan2014 to 2018Enrolled204ConditionsAlzheimer DiseaseArmsspinal fluid collection
3 · Its place in the literature

Who cites it

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

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  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

5 authors.

Aymric KisserliDepartment of Immunology, Reims University Hospitals, Robert Debré Hospital; Faculty of Medicine, LRN EA 4682, University of Reims Champagne-Ardenne.
Thierry TabaryDepartment of Immunology, Reims University Hospitals, Robert Debré Hospital; Faculty of Medicine, LRN EA 4682, University of Reims Champagne-Ardenne.
Jacques Henri Max CohenDepartment of Immunology, Reims University Hospitals, Robert Debré Hospital; Faculty of Medicine, LRN EA 4682, University of Reims Champagne-Ardenne; jhmcohen@gmail.com.
Valérie DuretDepartment of Immunology, Reims University Hospitals, Robert Debré Hospital; Faculty of Medicine, LRN EA 4682, University of Reims Champagne-Ardenne.
Rachid MahmoudiDepartment of Internal Medicine and Geriatrics, Reims University Hospitals, Maison Blanche Hospital; Faculty of Medicine, EA 3797, University of Reims Champagne-Ardenne.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Complement receptor 1 (CR1), a transmembrane glycoprotein that plays a key role in the innate immune system, is expressed on many cell types, but especially on red blood cells (RBCs). As a receptor for the complement components C3b and C4b, CR1 regulates the activation of the complement cascade and promotes the phagocytosis of immune complexes and cellular debris, as well as the amyloid-beta (Aβ) peptide in Alzheimer's disease (AD). Several studies have confirmed AD-associated single nucleotide polymorphisms (SNPs), as well as a copy-number variation (CNV) in the CR1 gene. Here, we describe an innovative method for determining the length polymorphism of the CR1 receptor. The receptor includes three domains, called long homologous repeats (LHR)-LHR-A, LHR-C, and LHR-D-and an n domain, LHR-B, where n is an integer between 0 and 3. Using a single pair of specific primers, the genetic material is used to amplify a first fragment of the LHR-B domain (the variant amplicon B) and a second fragment of the LHR-C domain (the invariant amplicon). The variant amplicon B and the invariant amplicon display differences at five nucleotides outside of the hybridization areas of said primers. The numbers of variant amplicons B and of invariant amplicons is deduced using a quantitative tool (high-resolution melting (HRM) curves), and the ratio of the variant amplicon B to the invariant amplicon differs according to the CR1 length polymorphism. This method provides several advantages over the canonical phenotype method, as it does not require fresh material and is cheaper, faster, and therefore applicable to larger populations. Thus, the use of this method should be helpful to better understand the role of CR1 isoforms in the pathogenesis of diseases such as AD.

Indexed as

Alzheimer DiseaseAmplified Fragment Length Polymorphism AnalysisDisease SusceptibilityDNAErythrocytesGenotypeHumansPhase TransitionPhenotypePolymorphism, Single NucleotideProtein IsoformsReceptors, ComplementSoftwareVideo RecordingDNAProtein IsoformsReceptors, Complement

Identifiers

PMID28745649
PMCPMC5612547

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Registered trials

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.