Evidence map›Paper›PMID 24586351›Full record

ArticlePloS one2014

Comparable autoantibody serum levels against amyloid- and inflammation-associated proteins in Parkinson's disease patients and controls.

Walter Maetzler, Anja Apel, Markus Langkamp, Christian Deuschle, Sarah Selina Dilger, Johannes Georg Stirnkorb, Claudia Schulte, Erwin Schleicher, Thomas Gasser, Daniela Berg

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Human leukocyte antigen in Parkinson's disease: A systematic review and meta-analysis of risk and clinical attributes.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
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  19. Anti-MAG autoantibodies are increased in Parkinson's disease but not in atypical parkinsonism.Journal of neural transmission (Vienna, Austria : 1996) · 2017
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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

10 authors at 4 institutions in 1 country.

Walter MaetzlerCenter of Neurology, Department of Neurodegeneration and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
Anja ApelCenter of Neurology, Department of Neurodegeneration and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
Markus LangkampMediagnost, Reutlingen, Germany.
Christian DeuschleCenter of Neurology, Department of Neurodegeneration and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
Sarah Selina DilgerCenter of Neurology, Department of Neurodegeneration and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
Johannes Georg StirnkorbCenter of Neurology, Department of Neurodegeneration and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
Claudia SchulteCenter of Neurology, Department of Neurodegeneration and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
Erwin SchleicherDepartment of Internal Medicine IV, University Hospital Tuebingen, Tuebingen, Germany.
Thomas GasserCenter of Neurology, Department of Neurodegeneration and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
Daniela BergCenter of Neurology, Department of Neurodegeneration and Hertie Institute for Clinical Brain Research, University of Tuebingen, Tuebingen, Germany ; DZNE, German Center for Neurodegenerative Diseases, University of Tuebingen, Tuebingen, Germany.
German Center for Neurodegenerative Diseases · DEHertie Institute for Clinical Brain Research · DEImmundiagnostik (Germany) · DEUniversity of Tübingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Naturally occurring autoantibodies (NAbs) against a number of potentially disease-associated cellular proteins, including Amyloid-beta1-42 (Abeta1-42), Alpha-synuclein (Asyn), myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG), and S100 calcium binding protein B (S100B) have been suggested to be associated with neurodegenerative disorders, in particular Alzheimer's (AD) and Parkinson's disease (PD). Whereas the (reduced) occurrence of specific NAbs in AD is widely accepted, previous literature examining the relation of these NAb titres between PD patients and controls, as well as comparing these levels with demographic and clinical parameters in PD patients have produced inconsistent findings. We therefore aimed, in a cross-sectional approach, to determine serum titres of the above NAbs in a cohort of 93 PD patients (31 of them demented) and 194 controls. Levels were correlated with demographic and clinical variables, cerebrospinal fluid Abeta1-42, total tau and phospho-tau levels, as well as with single nucleotide polymorphisms (SNPs) of genes which either have been reported to influence the immune system, the amyloid cascade or the occurrence of PD (ApoE, GSK3B, HLA-DRA, HSPA5, SNCA, and STK39). The investigated NAb titres were neither significantly associated with the occurrence of PD, nor with demographic and clinical parameters, neurodegenerative markers or genetic variables. These results argue against a major potential of blood-borne parameters of the adaptive immune system to serve as trait or state markers in PD.

Indexed as

alpha-SynucleinAmyloid beta-PeptidesApolipoproteins EAutoantibodiesCase-Control StudiesCross-Sectional StudiesEndoplasmic Reticulum Chaperone BiPEnzyme-Linked Immunosorbent AssayGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHeat-Shock ProteinsHLA-DR alpha-ChainsHumansMyelin Basic ProteinMyelin-Oligodendrocyte GlycoproteinParkinson Diseasealpha-SynucleinAmyloid beta-PeptidesApolipoproteins EAutoantibodiesEndoplasmic Reticulum Chaperone BiPGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanHeat-Shock ProteinsHLA-DR alpha-ChainsHSPA5 protein, humanMyelin Basic ProteinMyelin-Oligodendrocyte GlycoproteinProtein Serine-Threonine KinasesS100 Calcium Binding Protein beta SubunitSNCA protein, humanSTK39 protein, human

Identifiers

PMID24586351
PMCPMC3931625
OpenAlexW2016259443

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.