Evidence map›Paper›PMID 30708997›Full record

ReviewCells2019

Novel Immunotherapeutic Approaches to Target Alpha-Synuclein and Related Neuroinflammation in Parkinson's Disease.

Maria Angela Samis Zella, Judith Metzdorf, Friederike Ostendorf, Fabian Maass, Siegfried Muhlack, Ralf Gold, Aiden Haghikia, Lars Tönges

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Progress of Immunotherapies in Parkinson's Disease.CNS neuroscience & therapeutics · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Review
  10. Sequestration of Inflammation in Parkinson's Disease via Stem Cell Therapy.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. The Contribution of Microglia to Neuroinflammation in Parkinson's Disease.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Review
  20. Article
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

8 authors at 2 institutions in 1 country.

Maria Angela Samis ZellaDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. maria.zella@rub.de.
Judith MetzdorfDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. judith.metzdorf@rub.de.
Friederike OstendorfDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. friederike.ostendorf@googlemail.com.
Fabian MaassDepartment of Neurology, University Medical Center, 37075 Goettingen, Germany. fabian.maass@med.uni-goettingen.de.
Siegfried MuhlackDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. siegfried.muhlack@rub.de.
Ralf GoldDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. ralf.gold@rub.de.
Aiden HaghikiaDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. aiden.haghikia@rub.de.
Lars TöngesDepartment of Neurology, St. Josef-Hospital, Ruhr-University Bochum, 44791 Bochum, Germany. lars.toenges@rub.de.ORCID 0000-0001-6621-144X
St. Josef-Hospital · DEUniversity of Göttingen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiology of Parkinson's disease (PD) is significantly influenced by disease-causing changes in the protein alpha-Synuclein (aSyn). It can trigger and promote intracellular stress and thereby impair the function of dopaminergic neurons. However, these damage mechanisms do not only extend to neuronal cells, but also affect most glial cell populations, such as astroglia and microglia, but also T lymphocytes, which can no longer maintain the homeostatic CNS milieu because they produce neuroinflammatory responses to aSyn pathology. Through precise neuropathological examination, molecular characterization of biomaterials, and the use of PET technology, it has been clearly demonstrated that neuroinflammation is involved in human PD. In this review, we provide an in-depth overview of the pathomechanisms that aSyn elicits in models of disease and focus on the affected glial cell and lymphocyte populations and their interaction with pathogenic aSyn species. The interplay between aSyn and glial cells is analyzed both in the basic research setting and in the context of human neuropathology. Ultimately, a strong rationale builds up to therapeutically reduce the burden of pathological aSyn in the CNS. The current antibody-based approaches to lower the amount of aSyn and thereby alleviate neuroinflammatory responses is finally discussed as novel therapeutic strategies for PD.

Indexed as

Immunotherapyalpha-SynucleinBrainClinical Trials as TopicHumansInflammationParkinson Diseasealpha-Synucleinalpha-SynucleinimmunotherapyneuroinflammationParkinson’s disease

Identifiers

PMID30708997
PMCPMC6406239
OpenAlexW2912394781

What OpenQuestion holds

Textmetadata
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.