Evidence map›Paper›PMID 30874605›Full record

ArticleScientific reports2019

Antibody-mediated clearance of tau in primary mouse microglial cultures requires Fcγ-receptor binding and functional lysosomes.

Christian Rungsted Andersson, Jeppe Falsig, Jeffrey B Stavenhagen, Søren Christensen, Fredrik Kartberg, Nina Rosenqvist, Bente Finsen, Jan Torleif Pedersen

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.5field-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

46 citing papers in PubMed, 79 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
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  13. Proteolytic therapeutic modalities for amyloidoses: Insights into immunotherapy, PROTAC, and photo-oxygenation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  14. Review
  15. Article
  16. Targeting Endogenous Tau in Seeded Tauopathy Models Inhibits Tau Spread.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  17. Cellular and pathological functions of tau.Nature reviews. Molecular cell biology · 2024
    Review
  18. Review
  19. Review
  20. 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

8 authors at 2 institutions in 1 country.

Christian Rungsted AnderssonDepartment of Neurodegeneration, H. Lundbeck A/S, Copenhagen, Denmark. CRUA@lundbeck.com.
Jeppe FalsigDepartment of Neurodegeneration, H. Lundbeck A/S, Copenhagen, Denmark.
Jeffrey B StavenhagenBiology, Therachon, Basel, Switzerland.
Søren ChristensenBiologics, H. Lundbeck A/S, Copenhagen, Denmark.
Fredrik KartbergBiologics, H. Lundbeck A/S, Copenhagen, Denmark.
Nina RosenqvistDepartment of Neurodegeneration, H. Lundbeck A/S, Copenhagen, Denmark.
Bente FinsenNeurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, Odense, Denmark.
Jan Torleif PedersenDepartment of Neurodegeneration, H. Lundbeck A/S, Copenhagen, Denmark.
Lundbeck (Denmark) · DKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurodegenerative diseases such as Alzheimer's disease are characterized by the progressive spreading and accumulation of hyper-phosphorylated tau protein in the brain. Anti-tau antibodies have been shown to reduce tau pathology in in vivo models and antibody-mediated clearance of tau exerted by microglia has been proposed as a contributing factor. By subjecting primary microglia cultured in vitro to anti-phospho-tau antibodies in complex with pathological tau, we show that microglia internalise and degrade tau in a manner that is dependent on FcγR interaction and functional lysosomes. It has recently been discussed if anti-tau antibody effector-functions are required for induction of tau clearance. Using antibodies with compromised FcγR binding and non-compromised control antibodies we show that antibody effector functions are required for induction of microglial clearance of tau. Understanding the inflammatory consequences of targeting microglia using therapeutic antibodies is important when developing these molecules for clinical use. Using RNA sequencing, we show that treatment with anti-tau antibodies increases transcription of mRNA encoding pro-inflammatory markers, but that the mRNA expression profile of antibody-treated cells differ from the profile of LPS activated microglia. We further demonstrate that microglia activation alone is not sufficient to induce significant tau clearance.

Indexed as

Alzheimer DiseaseAnimalsAntibodiesBrainDisease Models, AnimalFemaleHumansLysosomesMaleMiceMice, TransgenicMicrogliaNeuronsPhosphorylationPrimary Cell CultureReceptors, IgGAntibodiesMapt protein, mouseReceptors, IgGtau Proteins

Identifiers

PMID30874605
PMCPMC6420568
OpenAlexW2921159745

What OpenQuestion holds

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LicenceCC BY
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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.