Evidence map›Paper›PMID 29538413›Full record

Trial reportPloS one2018

Functional autoantibodies in patients with different forms of dementia.

Gerd Wallukat, Harald Prüss, Johannes Müller, Ingolf Schimke

Erratum issuedOpen access · goldAbstract readClinical Trial
In one paragraph

Trial report in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 15% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. The role of autoantibodies in Alzheimer's disease: Pathogenetic connections or epiphenomena?Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Review
  5. Rare mixed dementia: A case report.World journal of radiology · 2025
    Article
  6. Review
  7. Observational
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Gerd WallukatBerlin Cures GmbH, Berlin, Germany.
Harald PrüssKlinik für Neurologie, Charité - Universitätsmedizin Berlin, Berlin, Germany.
Johannes MüllerBerlin Cures GmbH, Berlin, Germany.
Ingolf SchimkeBerlin Cures GmbH, Berlin, Germany.ORCID 0000-0002-0938-3154
Berlin Heart (Germany) · DEGerman Center for Neurodegenerative Diseases · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dementia in general and Alzheimer's disease in particular is increasingly seen in association with autoimmunity being causatively or supportively involved in the pathogenesis. Besides classic autoantibodies (AABs) present in dementia patients, there is the new autoantibody class called functional autoantibodies, which is directed against G-protein coupled receptors (GPCRs; GPCR-AABs) and are seen as pathogenic players. However, less is known about dementia patients' burden with functional autoantibodies. We present here for the first time a study analyzing the prevalence of GPCR-AABs in patients with different dementia forms such as unclassified, Lewy body, vascular and Alzheimer's dementia. We identified the GPCR-AABs' specific targets on the receptors and introduced a neutralization strategy for GPCR-AABs. Patients with Alzheimer’s and vascular dementia carried GPCR-AABs targeting the second loop of the alpha1- and the first loop of the beta2-adrenergic receptors (α1-AABs; β2-AABs). The majority of patients with Lewy body dementia lacked any of the GPCR-AABs. In vitro, the function of the dementia-associated GPCR-AABs could be neutralized by the aptamer BC007. Due to the presence of GPCR-AABs in dementia patients mainly in those suffering from Alzheimer's and vascular dementia, the orchestra of immune players in these dementia forms, so far preferentially represented by the classic autoantibodies, should be supplemented by functional autoantibodies. As dementia-associated functional autoantibodies could be neutralized by the aptamer BC007, the first step was taken for a new in vivo treatment option in dementia patients who were positive for GPCR-AABs.

Indexed as

AutoantibodiesAutoimmune DiseasesDementiaAgedFemaleHumansMaleMiddle AgedProtein DomainsReceptors, Adrenergic, beta-2AutoantibodiesReceptors, Adrenergic, beta-2

Identifiers

PMID29538413
PMCPMC5851545
OpenAlexW2792942476

What OpenQuestion holds

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LicenceCC BY
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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.