Evidence map›Paper›PMID 27647497›Full record

ArticleNature communications2016

Delayed glial clearance of degenerating axons in aged Drosophila is due to reduced PI3K/Draper activity.

Maria D Purice, Sean D Speese, Mary A Logan

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 57 citations in OpenAlex.

  1. Progressive behavioral and cognitive decline inbioRxiv : the preprint server for biology · 2026
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  8. Glial Regulation of Circuit Wiring, Firing, and Expiring in theCold Spring Harbor perspectives in biology · 2024
    Review
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  11. Article
  12. Impairment of the Glial Phagolysosomal System Drives Prion-Like Propagation in aThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. eLife · 2022
    Article
  19. Article
  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

3 authors at 1 institution in 1 country.

Maria D PuriceJungers Center for Neurosciences Research, Department of Neurology, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97239, USA.
Sean D SpeeseJungers Center for Neurosciences Research, Department of Neurology, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97239, USA.
Mary A LoganJungers Center for Neurosciences Research, Department of Neurology, Oregon Health and Science University, 3181 Southwest Sam Jackson Park Road, Portland, Oregon 97239, USA.
Center for Neurosciences · US

Funding

Resource Component: Acquisition, maintenance and distribution of Drosophila stocksP40OD018537 · OD · TRUSTEES OF INDIANA UNIVERSITY · PI Annette L. Parks · 2014 to 2026
$13.5M
Neuroscience of AgingT32AG023477 · NIA · OREGON HEALTH & SCIENCE UNIVERSITY · PI URBANSKI, HENRYK F · 2005 to 2015
$2.4M
Role of Insulin-like Signaling in Glial Responses to Axon DegenerationR01NS079387 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI LOGAN, MARY ALLISON · 2012 to 2016
$1.6M
Jungers Center New Faculty Recruitment in Genetic Models of Axonal DegenerationP30NS069346 · NINDS · OREGON HEALTH & SCIENCE UNIVERSITY · PI BOURDETTE, DENNIS NEIL · 2009 to 2010
$1.3M
NIA NIH HHS T32 AG023477NIH HHS P40 OD018537NINDS NIH HHS P30 NS069346NINDS NIH HHS R01 NS079387
6 · The paper itself

Abstract

Advanced age is the greatest risk factor for neurodegenerative disorders, but the mechanisms that render the senescent brain vulnerable to disease are unclear. Glial immune responses provide neuroprotection in a variety of contexts. Thus, we explored how glial responses to neurodegeneration are altered with age. Here we show that glia-axon phagocytic interactions change dramatically in the aged Drosophila brain. Aged glia clear degenerating axons slowly due to low phosphoinositide-3-kinase (PI3K) signalling and, subsequently, reduced expression of the conserved phagocytic receptor Draper/MEGF10. Importantly, boosting PI3K/Draper activity in aged glia significantly reverses slow phagocytic responses. Moreover, several hours post axotomy, early hallmarks of Wallerian degeneration (WD) are delayed in aged flies. We propose that slow clearance of degenerating axons is mechanistically twofold, resulting from deferred initiation of axonal WD and reduced PI3K/Draper-dependent glial phagocytic function. Interventions that boost glial engulfment activity, however, can substantially reverse delayed clearance of damaged neuronal debris.

Indexed as

AgingAnimalsAxonsAxotomyDrosophilaDrosophila ProteinsMembrane ProteinsNeurogliaPhagocytosisPhosphatidylinositol 3-KinasesSTAT Transcription FactorsTOR Serine-Threonine KinasesDrosophila Proteinsdrpr protein, DrosophilaMembrane ProteinsPhosphatidylinositol 3-KinasesStat92E protein, DrosophilaSTAT Transcription Factorstarget of rapamycin protein, DrosophilaTOR Serine-Threonine Kinases

Identifiers

PMID27647497
PMCPMC5034330
OpenAlexW2522017513

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.