Evidence map›Paper›PMID 35701430›Full record

ArticleNPJ Parkinson's disease2022

Angiotensin type-1 receptor and ACE2 autoantibodies in Parkinson´s disease.

Carmen M Labandeira, Maria A Pedrosa, Aloia Quijano, Rita Valenzuela, Pablo Garrido-Gil, Mariña Sanchez-Andrade, Juan A Suarez-Quintanilla, Ana I Rodriguez-Perez, Jose L Labandeira-Garcia

Open access · goldAbstract read
In one paragraph

Article in NPJ Parkinson's disease, 2022. 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
3.9field-weighted citation impact, top 5% 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, 44 citations in OpenAlex.

  1. Review
  2. Article
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  4. ACE2: Friend or Foe in Post-COVID-19 Neurodegeneration?International journal of molecular sciences · 2025
    Review
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  8. Article
  9. Autoantibodies targeting angiotensin-converting enzyme 2 are prevalent and not induced by SARS-CoV-2 infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  12. Review
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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

9 authors at 2 institutions in 1 country.

Carmen M Labandeira *Research Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.
Maria A Pedrosa *Research Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.
Aloia QuijanoResearch Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.
Rita ValenzuelaResearch Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.
Pablo Garrido-GilResearch Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.ORCID http://orcid.org/0000-0001-7734-8783
Mariña Sanchez-AndradeObstetric Service, University Clinical Hospital of Santiago de Compostela, Santiago de Compostela, Spain.
Juan A Suarez-QuintanillaPrimary Health-Care Unit Fontiñas, IDIS, Santiago de Compostela, Spain.
Ana I Rodriguez-PerezResearch Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain. anai.rodriguez@usc.es.ORCID http://orcid.org/0000-0003-1354-8799
Jose L Labandeira-GarciaResearch Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain. joseluis.labandeira@usc.es.
Universidade de Santiago de Compostela · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ES

Funding

Ministerio de Economía y Competitividad (Ministry of Economy and Competitiveness) RTI2018-098830-B-I00Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) RD21/0017/0031
6 · The paper itself

Abstract

The role of autoimmunity in neurodegeneration has been increasingly suggested. The renin-angiotensin system (RAS) autoantibodies play a major role in several peripheral inflammatory processes. Dysregulation of brain RAS has been involved in neuroinflammation and neurodegeneration. We aimed to know whether angiotensin type-1 receptor (AT1) autoantibodies (AT1 agonists) and angiotensin-converting enzyme 2 (ACE2) autoantibodies (ACE2 antagonists) may be involved in Parkinson's disease (PD) progression and constitute a new therapeutical target. Both AT1 and ACE2 serum autoantibodies were higher in a group of 117 PD patients than in a group of 106 controls. Serum AT1 autoantibodies correlated with several cytokines, particularly Tumor Necrosis Factor Ligand Superfamily Member 14 (TNFSF14, LIGHT), and 27-hydroxycholesterol levels. Serum ACE2 autoantibodies correlated with AT1 autoantibodies. Both autoantibodies were found in cerebrospinal fluid (CSF) of four PD patients with CSF samples. Consistent with the observations in patients, experimental dopaminergic degeneration, induced by 6-hydroxydopamine, increased levels of autoantibodies in serum and CSF in rats, as well as LIGHT levels and transglutaminase activity in rat substantia nigra. In cultures, administration of AT1 autoantibodies enhanced dopaminergic neuron degeneration and increased levels of neuroinflammation markers, which was inhibited by the AT1 antagonist candesartan. The results suggest dysregulation of RAS autoantibodies as a new mechanism that can contribute to PD progression. Therapeutical strategies blocking the production, or the effects of these autoantibodies may be useful for PD treatment, and the results further support repurposing AT1 blockers (ARBs) as treatment against PD progression.

Identifiers

PMID35701430
PMCPMC9198025
OpenAlexW4282842476

What OpenQuestion holds

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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.