Evidence map›Paper›PMID 25972570›Full record

ArticleDiabetes2015

Detection of Antibodies Directed to the N-Terminal Region of GAD Is Dependent on Assay Format and Contributes to Differences in the Specificity of GAD Autoantibody Assays for Type 1 Diabetes.

Alistair J K Williams, Vito Lampasona, Michael Schlosser, Patricia W Mueller, David L Pittman, William E Winter, Beena Akolkar, Rebecca Wyatt, Cristina Brigatti, Stephanie Krause and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Diabetes, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

26 citing papers in PubMed, 47 citations in OpenAlex.

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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

12 authors at 5 institutions in 2 countries.

Alistair J K WilliamsSchool of Clinical Sciences, University of Bristol, Bristol, U.K. a.j.k.williams@bristol.ac.uk.
Vito LampasonaDivision of Genetics and Cell Biology, San Raffaele Scientific Institute, Milan, Italy.
Michael SchlosserDepartment of Medical Biochemistry and Molecular Biology and Institute of Pathophysiology, University Medical Center of Greifswald, Karlsburg, Germany.
Patricia W MuellerMolecular Risk Assessment Laboratory, Centers for Disease Control and Prevention, Atlanta, GA.
David L PittmanDepartment of Pathology, University of Florida, Gainesville, FL.
William E WinterDepartment of Pathology, University of Florida, Gainesville, FL.
Beena AkolkarDivision of Diabetes, Endocrinology, and Metabolic Diseases, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD.
Rebecca WyattSchool of Clinical Sciences, University of Bristol, Bristol, U.K.
Cristina BrigattiDiabetes Research Institute, San Raffaele Scientific Institute, Milan, Italy.
Stephanie KrauseInstitute of Diabetes Research, Helmholtz Zentrum München, and Forschergruppe Diabetes, Klinikum rechts der Isar, Technische Universität München, Neuherberg, Germany.
Peter AchenbachInstitute of Diabetes Research, Helmholtz Zentrum München, and Forschergruppe Diabetes, Klinikum rechts der Isar, Technische Universität München, Neuherberg, Germany.
Participating Laboratories
University of Florida · USCenters for Disease Control and Prevention · USKlinikum rechts der Isar · DENational Institute of Diabetes and Digestive and Kidney Diseases · USTechnical University of Munich · DE

Funding

PHS HHS PL105-33PHS HHS PL106-310PHS HHS PL106-554PHS HHS PL107-360
6 · The paper itself

Abstract

GAD autoantibodies (GADAs) are sensitive markers of islet autoimmunity and type 1 diabetes. They form the basis of robust prediction models and are widely used for the recruitment of subjects at high risk of type 1 diabetes to prevention trials. However, GADAs are also found in many individuals at low risk of diabetes progression. To identify the sources of diabetes-irrelevant GADA reactivity, we analyzed data from the 2009 and 2010 Diabetes Autoantibody Standardization Program GADA workshop and found that binding of healthy control sera varied according to assay type. The characterization of control sera found positive by radiobinding assay (RBA), but negative by ELISA, showed that many of these sera reacted to epitopes in the N-terminal region of the molecule. This finding prompted development of an N-terminally truncated GAD65 radiolabel, (35)S-GAD65(96-585), which improved the performance of most GADA RBAs participating in an Islet Autoantibody Standardization Program GADA substudy. These detailed workshop comparisons have identified a source of disease-irrelevant signals in GADA RBAs and suggest that N-terminally truncated GAD labels will enable more specific measurement of GADAs in type 1 diabetes.

Indexed as

Enzyme-Linked Immunosorbent AssayRadioligand AssayAdolescentAdultAutoantibodiesCase-Control StudiesChildDiabetes Mellitus, Type 1EpitopesFemaleGlutamate DecarboxylaseHumansMaleMiddle AgedSensitivity and SpecificityYoung AdultAutoantibodiesEpitopesGlutamate Decarboxylase

Identifiers

PMID25972570
PMCPMC4542444
OpenAlexW2167007291

What OpenQuestion holds

Textmetadata
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.