Evidence map›Paper›PMID 33628204›Full record

ArticleFrontiers in immunology2020

Identification of Neuronal Pentraxins as Synaptic Binding Partners of C1q and the Involvement of NP1 in Synaptic Pruning in Adult Mice.

Réka Á Kovács, Henrietta Vadászi, Éva Bulyáki, György Török, Vilmos Tóth, Dominik Mátyás, Judit Kun, Éva Hunyadi-Gulyás, Flóra Zsófia Fedor, Ádám Csincsi and 7 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

31 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. The neuroimmune system and cognition.Nature immunology · 2026
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. C5aR1 signaling promotes region- and age-dependent synaptic pruning in models of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Article
  18. Review
  19. Article
  20. As a Potential Therapeutic Target, C1q Induces Synapse Loss Via Inflammasome-activating Apoptotic and Mitochondria Impairment Mechanisms in Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023
    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

17 authors at 6 institutions in 1 country.

Réka Á KovácsELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Henrietta VadásziELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Éva BulyákiELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
György TörökMolecular Cell Biology Research Group, Institute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences Centre of Excellence, Budapest, Hungary.
Vilmos TóthELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Dominik MátyásELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Judit KunELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Éva Hunyadi-GulyásLaboratory of Proteomics Research, Biological Research Centre, Eötvös Loránd Research Network (ELKH), Szeged, Hungary.
Flóra Zsófia FedorELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Ádám CsincsiComplement Research Group, Department of Immunology, ELTE Eötvös Loránd University, Budapest, Hungary.
Katalin MedzihradszkyLaboratory of Proteomics Research, Biological Research Centre, Eötvös Loránd Research Network (ELKH), Szeged, Hungary.
László HomolyaMolecular Cell Biology Research Group, Institute of Enzymology, Research Center for Natural Sciences, Hungarian Academy of Sciences Centre of Excellence, Budapest, Hungary.
Gábor JuhászELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Katalin A KékesiELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Mihály JózsiComplement Research Group, Department of Immunology, ELTE Eötvös Loránd University, Budapest, Hungary.
Balázs A GyörffyELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
József KardosELTE NAP Neuroimmunology Research Group, Department of Biochemistry, Institute of Biology, ELTE Eötvös Loránd University, Budapest, Hungary.
Eötvös Loránd University · HUHungarian Academy of Sciences · HUHungarian Research NetworkHUN-REN Szegedi Biológiai Kutatóközpont · HUInstitute of Molecular Life Sciences · HUUniversity of Pannonia · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elements of the immune system particularly that of innate immunity, play important roles beyond their traditional tasks in host defense, including manifold roles in the nervous system. Complement-mediated synaptic pruning is essential in the developing and healthy functioning brain and becomes aberrant in neurodegenerative disorders. C1q, component of the classical complement pathway, plays a central role in tagging synapses for elimination; however, the underlying molecular mechanisms and interaction partners are mostly unknown. Neuronal pentraxins (NPs) are involved in synapse formation and plasticity, moreover, NP1 contributes to cell death and neurodegeneration under adverse conditions. Here, we investigated the potential interaction between C1q and NPs, and its role in microglial phagocytosis of synapses in adult mice. We verified

Indexed as

PhagocytosisAlzheimer DiseaseAnimalsComplement C1qComplement C4C-Reactive ProteinMaleMiceMicrogliaNerve Tissue ProteinsPentraxinsSynapsesComplement C1qComplement C4C-Reactive ProteinNerve Tissue ProteinsPentraxinscomplement classical pathwaycomplement component C1qflow cytometryimmunostainingmicroglial phagocytosisneuronal pentraxinsynaptic pruningsynaptosome

Identifiers

PMID33628204
PMCPMC7897678
OpenAlexW3127928580

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.