Evidence map›Paper›PMID 35742998›Full record

ArticleInternational journal of molecular sciences2022

Alpha-Synuclein Autoimmune Decline in Prodromal Multiple System Atrophy and Parkinson's Disease.

Jonas Folke, Emil Bergholt, Bente Pakkenberg, Susana Aznar, Tomasz Brudek

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

8 citing papers in PubMed, 8 citations in OpenAlex.

  1. Cutaneous alpha-synuclein deposition informs autonomic function in individuals with early-stage multiple system atrophy.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Molecular Mechanisms Underlying Chronic and Degenerative Diseases.International journal of molecular sciences · 2023
    Article
  7. Article
  8. B Lymphocytes in Parkinson's Disease.Journal of Parkinson's disease · 2022
    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

5 authors at 2 institutions in 1 country.

Jonas FolkeCentre for Neuroscience & Stereology, Department of Neurology, Copenhagen University Hospital, Bispebjerg-Frederiksberg Hospital, DK-2400 Copenhagen NV, Denmark.ORCID 0000-0002-0940-3098
Emil BergholtCentre for Neuroscience & Stereology, Department of Neurology, Copenhagen University Hospital, Bispebjerg-Frederiksberg Hospital, DK-2400 Copenhagen NV, Denmark.
Bente PakkenbergCentre for Neuroscience & Stereology, Department of Neurology, Copenhagen University Hospital, Bispebjerg-Frederiksberg Hospital, DK-2400 Copenhagen NV, Denmark.
Susana AznarCentre for Neuroscience & Stereology, Department of Neurology, Copenhagen University Hospital, Bispebjerg-Frederiksberg Hospital, DK-2400 Copenhagen NV, Denmark.
Tomasz BrudekCentre for Neuroscience & Stereology, Department of Neurology, Copenhagen University Hospital, Bispebjerg-Frederiksberg Hospital, DK-2400 Copenhagen NV, Denmark.
Frederiksberg Hospital · DKUniversity of Copenhagen · DK

Funding

HSRD VA TPP 10-008
6 · The paper itself

Abstract

Multiple-system trophy (MSA) and Parkinson's Disease (PD) are both progressive, neurodegenerative diseases characterized by neuropathological deposition of aggregated alpha-synuclein (αSyn). The causes behind this aggregation are still unknown. We have reported aberrancies in MSA and PD patients in naturally occurring autoantibodies (nAbs) against αSyn (anti-αSyn-nAbs), which are important partakers in anti-aggregatory processes, immune-mediated clearance, and anti-inflammatory functions. To elaborate further on the timeline of autoimmune aberrancies towards αSyn, we investigated here the Immunoglobulin (Ig) affinity profile and subclass composition (IgG-total, IgG1-4 and IgM) of anti-αSyn-nAbs in serum samples from prodromal (p) phases of MSA and PD. Using an electrochemiluminescence competition immunoassay, we confirmed that the repertoire of high-affinity anti-αSyn-nAbs is significantly reduced in pMSA and pPD. Further, we demonstrated that pPD had increased anti-αSyn IgG-total levels compared to pMSA and controls, concordant with increased anti-αSyn IgG1 levels in pPD. Anti-αSyn IgG2 and IgG4 levels were reduced in pMSA and pPD compared with controls, whereas anti-αSyn IgG3 levels were reduced in pMSA compared to pPD and controls. The results indicate that the impaired reactivity towards αSyn occurs prior to disease onset. The apparent lack of high-affinity anti-αSyn nAbs may result in reduced clearance of αSyn, leading to aggregation of the protein. Thus, this study provides novel insights into possible causes behind the pathogenesis in synucleinopathies such as MSA and PD.

Indexed as

Multiple System AtrophyParkinson Diseasealpha-SynucleinAutoantibodiesHumansImmunoglobulin Galpha-SynucleinAutoantibodiesImmunoglobulin Galpha-synucleinmultiple system atrophynaturally occurring autoantibodies (nAbs)Parkinson’s diseaseprodromal

Identifiers

PMID35742998
PMCPMC9224313
OpenAlexW4282553314

What OpenQuestion holds

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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.