Evidence map›Paper›PMID 38368444›Full record

ArticleNPJ Parkinson's disease2024

Angiotensin type 1 receptor activation promotes neuronal and glial alpha-synuclein aggregation and transmission.

Lucia Lage, Ana I Rodriguez-Perez, Begoña Villar-Cheda, Jose L Labandeira-Garcia, Antonio Dominguez-Meijide

Open access · goldAbstract read
In one paragraph

Article in NPJ Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Ang II-mediated effects on BBB integrity in psychiatric and neurological disorders.Progress in neuro-psychopharmacology & biological psychiatry · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Fasudil inhibits α-synuclein aggregation through ROCK-inhibition-mediated mechanisms.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  10. Article
  11. Article
  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

5 authors at 1 institution in 1 country.

Lucia LageCellular and Molecular Neurobiology of Parkinson's disease, Research Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.
Ana I Rodriguez-PerezCellular and Molecular Neurobiology of Parkinson's disease, Research Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.ORCID http://orcid.org/0000-0003-1354-8799
Begoña Villar-ChedaCellular and Molecular Neurobiology of Parkinson's disease, Research Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain.ORCID http://orcid.org/0000-0002-9857-0524
Jose L Labandeira-GarciaCellular and Molecular Neurobiology of Parkinson's disease, Research Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain. joseluis.labandeira@usc.es.ORCID http://orcid.org/0000-0002-8243-9791
Antonio Dominguez-MeijideCellular and Molecular Neurobiology of Parkinson's disease, Research Center for Molecular Medicine and Chronic diseases (CIMUS), IDIS, University of Santiago de Compostela, Santiago de Compostela, Spain. antonio.meijide@usc.es.ORCID http://orcid.org/0000-0002-8666-0223
Universidade de Santiago de Compostela · ES

Funding

Consellería de Cultura, Educación e Ordenación Universitaria, Xunta de Galicia (Ministry of Culture, Education and University Planning, Government of Galicia) ED431C 2022/41Ministerio de Economía y Competitividad (Ministry of Economy and Competitiveness) PID2021-126848NB-I00Ministerio de Economía y Competitividad (Ministry of Economy and Competitiveness) PLEC2022-009401Ministry of Economy and Competitiveness | Instituto de Salud Carlos III (Institute of Health Carlos III) RD21/0017/0031
6 · The paper itself

Abstract

The brain renin-angiotensin system (RAS) has been related to dopaminergic degeneration, and high expression of the angiotensin II (AngII) type 1 receptor (AT1) gene is a marker of the most vulnerable neurons in humans. However, it is unknown whether AngII/AT1 overactivation affects α-synuclein aggregation and transmission. In vitro, AngII/AT1 activation increased α-synuclein aggregation in dopaminergic neurons and microglial cells, which was related to AngII-induced NADPH-oxidase activation and intracellular calcium raising. In mice, AngII/AT1 activation was involved in MPTP-induced increase in α-synuclein expression and aggregation, as they significantly decreased in mice treated with the AT1 blocker telmisartan and AT1 knockout mice. Cell co-cultures (transwells) revealed strong transmission of α-synuclein from dopaminergic neurons to astrocytes and microglia. AngII induced a higher α-synuclein uptake by microglial cells and an increase in the transfer of α-synuclein among astroglial cells. However, AngII did not increase the release of α-synuclein by neurons. The results further support brain RAS dysregulation as a major mechanism for the progression of Parkinson's disease, and AT1 inhibition and RAS modulation as therapeutic targets.

Identifiers

PMID38368444
PMCPMC10874459
OpenAlexW4391896821

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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.