Evidence map›Paper›PMID 30134156›Full record

ArticleCell reports2018

Living Neurons with Tau Filaments Aberrantly Expose Phosphatidylserine and Are Phagocytosed by Microglia.

Jack Brelstaff, Aviva M Tolkovsky, Bernardino Ghetti, Michel Goedert, Maria Grazia Spillantini

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed
9.0field-weighted citation impact, top 1% 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

122 citing papers in PubMed, 193 citations in OpenAlex.

  1. Synthetic viral RNA mimetics induce neuronal loss through microglial phagocytosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  10. Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026
    Review
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  19. Neuroinflammation in Alzheimer disease.Nature reviews. Immunology · 2025
    Review
  20. Senescent brain cell types in Alzheimer's disease: Pathological mechanisms and therapeutic opportunities.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review

62 more citing papers are in PubMed but not listed here.

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 3 institutions in 2 countries.

Jack BrelstaffDepartment of Clinical Neurosciences, Clifford Allbutt Building, University of Cambridge, Cambridge, CB2 0AH, UK.
Aviva M TolkovskyDepartment of Clinical Neurosciences, Clifford Allbutt Building, University of Cambridge, Cambridge, CB2 0AH, UK. Electronic address: amt1004@cam.ac.uk.
Bernardino GhettiDepartment of Pathology and Laboratory Medicine, Indiana University, Indianapolis, IN, USA.
Michel GoedertMedical Research Council Laboratory of Molecular Biology, Cambridge CB2 0QH, UK.
Maria Grazia SpillantiniDepartment of Clinical Neurosciences, Clifford Allbutt Building, University of Cambridge, Cambridge, CB2 0AH, UK. Electronic address: mgs11@cam.ac.uk.
University of Cambridge · GBIndiana University – Purdue University Indianapolis · USMedical Research Council · GB

Funding

Research Education ComponentP30AG010133 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SAYKIN, ANDREW J · 1991 to 2020
$37.3M
Medical Research Council MC_U105184291National Centre for the Replacement, Refinement and Reduction of Animals in Research NC/L000741/1NIA NIH HHS P30 AG010133
6 · The paper itself

Abstract

Tau protein forms insoluble filamentous inclusions that are closely associated with nerve cell death in many neurodegenerative diseases. How neurons die in these tauopathies is unclear. We report that living neurons with tau inclusions from P301S-tau mice expose abnormally high amounts of phosphatidylserine because of the production of reactive oxygen species (ROS). Consequently, co-cultured phagocytes (BV2 cells or primary microglia) identify and phagocytose the living neurons, thereby engulfing insoluble tau inclusions. To facilitate engulfment, neurons induce contacting microglia to secrete the opsonin milk-fat-globule EGF-factor-8 (MFGE8) and nitric oxide (NO), whereas neurons with tau inclusions are rescued when MFGE8 or NO production is prevented. MFGE8 expression is elevated in transgenic P301S-tau mouse brains with tau inclusions and in tau inclusion-rich brain regions of several human tauopathies, indicating shared mechanisms of disease. Preventing phagocytosis of living neurons will preserve them for treatments that inhibit tau aggregation and toxicity.

Indexed as

AnimalsHumansMiceMicrogliaNeuronsPhagocytosisPhosphatidylserinestau ProteinsPhosphatidylserinestau Proteinscell deathMFGE8microglianeurodegenerationneuroinflammationnitric oxidephagocytosisphosphatidylserinetautauopathies

Identifiers

PMID30134156
PMCPMC6161320
OpenAlexW2888349482

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.