Evidence map›Paper›PMID 33408815›Full record

ArticleJournal of extracellular vesicles2020

Astrocytes deliver CK1 to neurons via extracellular vesicles in response to inflammation promoting the translation and amyloidogenic processing of APP.

Zhigang Li, Mohammed Moniruzzaman, Raha M Dastgheyb, Seung-Wan Yoo, Meina Wang, Hongbo Hao, Jia Liu, Patrizia Casaccia, Carlos Nogueras-Ortiz, Dimitrios Kapogiannis and 2 more

Open access · goldAbstract read
In one paragraph

Article in Journal of extracellular vesicles, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 10% 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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
  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

12 authors at 5 institutions in 1 country.

Zhigang LiDepartment of Neurology, Richard T. Johnson Division of Neuroimmunology and Neurological Infections Johns Hopkins University School of Medicine Baltimore Maryland USA.
Mohammed MoniruzzamanDepartment of Neurology, Richard T. Johnson Division of Neuroimmunology and Neurological Infections Johns Hopkins University School of Medicine Baltimore Maryland USA.
Raha M DastgheybDepartment of Neurology, Richard T. Johnson Division of Neuroimmunology and Neurological Infections Johns Hopkins University School of Medicine Baltimore Maryland USA.
Seung-Wan YooDepartment of Neurology, Richard T. Johnson Division of Neuroimmunology and Neurological Infections Johns Hopkins University School of Medicine Baltimore Maryland USA.
Meina WangDepartment of Neurology, Richard T. Johnson Division of Neuroimmunology and Neurological Infections Johns Hopkins University School of Medicine Baltimore Maryland USA.
Hongbo HaoAdvanced Science Research Center at the Graduate Center, Neuroscience Initiative City University of New York New York New York USA.
Jia LiuAdvanced Science Research Center at the Graduate Center, Neuroscience Initiative City University of New York New York New York USA.
Patrizia CasacciaAdvanced Science Research Center at the Graduate Center, Neuroscience Initiative City University of New York New York New York USA.
Carlos Nogueras-OrtizLaboratory of Clinical Investigation National Institute on Aging Baltimore Maryland USA.
Dimitrios KapogiannisLaboratory of Clinical Investigation National Institute on Aging Baltimore Maryland USA.
Barbara S SlusherDepartment of Neurology, Richard T. Johnson Division of Neuroimmunology and Neurological Infections Johns Hopkins University School of Medicine Baltimore Maryland USA.
Norman J HaugheyDepartment of Neurology, Richard T. Johnson Division of Neuroimmunology and Neurological Infections Johns Hopkins University School of Medicine Baltimore Maryland USA.
Johns Hopkins Medicine · USCUNY Advanced Science Research Center · USJohns Hopkins University · USNational Institute on Aging · USThe Graduate Center, CUNY · US

Funding

Therapeutic CoreP30MH075673 · NIMH · JOHNS HOPKINS UNIVERSITY · PI Leah Helane Rubin · 2006 to 2026
$33.2M
Surrogate Marker CoreP01MH105280 · NIMH · JOHNS HOPKINS UNIVERSITY · PI SACKTOR, NED C · 2015 to 2019
$6.5M
Mechanisms of Neuroinflammation in HANDR01MH077542 · NIMH · JOHNS HOPKINS UNIVERSITY · PI HAUGHEY, NORMAN J · 2007 to 2016
$3.4M
Regulation of Exosome Secretion as a novel therapeutic approach for Alzheimer's DiseaseR01AG059799 · NIA · JOHNS HOPKINS UNIVERSITY · PI SLUSHER, BARBARA STAUCH, TSUKAMOTO, TAKASHI · 2018 to 2022
$2.4M
Exosomes:From biogenesis and secretion to the early pathogenesis of Alzheimer's diseaseR01AG057420 · NIA · JOHNS HOPKINS UNIVERSITY · PI HAUGHEY, NORMAN J · 2017 to 2021
$2.0M
Dysregualtion of gliotransmission in models of neuroHIVR01MH110246 · NIMH · JOHNS HOPKINS UNIVERSITY · PI HAUGHEY, NORMAN J · 2016 to 2020
$2.0M
NIA NIH HHS R01 AG057420NIA NIH HHS R01 AG059799NIMH NIH HHS P01 MH105280NIMH NIH HHS P30 MH075673NIMH NIH HHS R01 MH077542NIMH NIH HHS R01 MH110246
6 · The paper itself

Abstract

Chronic inflammation is thought to contribute to the early pathogenesis of Alzheimer's disease (AD). However, the precise mechanism by which inflammatory cytokines promote the formation and deposition of Aβ remains unclear. Available data suggest that applications of inflammatory cytokines onto isolated neurons do not promote the formation of Aβ, suggesting an indirect mechanism of action. Based on evidence astrocyte derived extracellular vesicles (astrocyte derived EVs) regulate neuronal functions, and data that inflammatory cytokines can modify the molecular cargo of astrocyte derived EVs, we sought to determine if IL-1β promotes the formation of Aβ indirectly through actions of astrocyte derived EVs on neurons. The production of Aβ was increased when neurons were exposed to astrocyte derived EVs shed in response to IL-1β (astrocyte derived EV-IL-1β). The mechanism for this effect involved an enrichment of Casein kinase 1 (CK1) in astrocyte derived EV-IL-1β. This astrocyte derived CK1 was delivered to neurons where it formed a complex with neuronal APC and GSK3 to inhibit the β-catenin degradation. Stabilized β-catenin translocated to the nucleus and bound to

Indexed as

AgedAged, 80 and overAlzheimer DiseaseAmyloidAmyloid beta-Protein PrecursorAnimalsAstrocytesCase-Control StudiesCasein Kinase IExtracellular VesiclesFemaleFragile X Messenger Ribonucleoprotein 1Glycogen Synthase Kinase 3HumansInflammationInterleukin-1betaAmyloidAmyloid beta-Protein PrecursorCasein Kinase IFMR1 protein, humanFragile X Messenger Ribonucleoprotein 1Glycogen Synthase Kinase 3Interleukin-1betaamyloid betaastrocytes‐neurons cross talkextracellular vesiclesinflammation

Identifiers

PMID33408815
PMCPMC7775567
OpenAlexW3120886928

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.