Evidence map›Paper›PMID 21693708›Full record

ArticleThe Journal of biological chemistry2011

Involvement of the Fc gamma receptor in a chronic N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of dopaminergic loss.

Arman Lira, Jerzy Kulczycki, Ruth Slack, Hymie Anisman, David S Park

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

11 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. The immunology of Parkinson's disease.Seminars in immunopathology · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. Neurodegeneration by activation of the microglial complement-phagosome pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  8. Microglia development and function.Annual review of immunology · 2014
    Review
  9. Article
  10. Article
  11. 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 2 countries.

Arman LiraDepartment of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.
Jerzy KulczyckiInstitute of Neuroscience, Carleton University, Ottawa, Ontario K1S 5B6, Canada, and.
Ruth SlackDepartment of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.
Hymie AnismanInstitute of Neuroscience, Carleton University, Ottawa, Ontario K1S 5B6, Canada, and.
David S ParkDepartment of Cellular Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada,; Department of Cogno-Mechatronics Engineering, Pusan National University, Korea. Electronic address: dpark@uottawa.ca.
University of Ottawa · CACarleton University · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Although there is growing evidence for a role of the innate immune response in Parkinson's disease, the nature of any humoral response in dopaminergic degeneration is uncertain. Here we report on a protracted N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model of dopaminergic death that potentially allows a more full adaptive humoral response to develop. Rag2 mutant mice that lack the full adaptive response (deficient in both T and B cells) are resistant to dopaminergic death and behavioral deficiencies in this model. These mice are resensitized after reconstitution with WT splenocytes. To more directly provide evidence for humoral/IgG involvement, we show that deficiency of Fcγ receptors, which are critical for activation of macrophages/microglia by binding to IgGs, is also protective in this protracted model. FcγR-deficient mice display improved behavior and impaired microglial activation. Interestingly, however, Rag2 mutant but not FcγR-deficient mice are resistant to a more standard N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine paradigm where death is more rapid. Taken together, these data indicate that, provided sufficient time, the humoral arm of the adaptive immune system can play a critical functional role in modulating the microglial response to dopaminergic degeneration and suggest that this humoral component may participate in degeneration in Parkinson's disease.

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnimalsCell DeathDisease Models, AnimalDNA-Binding ProteinsImmunoglobulin GMiceMice, KnockoutMPTP PoisoningNeurotoxinsParkinson Disease, SecondaryReceptors, IgG1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineDNA-Binding ProteinsImmunoglobulin GNeurotoxinsRag2 protein, mouseReceptors, IgG

Identifiers

PMID21693708
PMCPMC3190686
OpenAlexW1971415136

What OpenQuestion holds

Textmetadata
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.