Evidence map›Paper›PMID 35426061›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2022

Pathogenic Extracellular Vesicle (EV) Signaling in Amyotrophic Lateral Sclerosis (ALS).

Gloria Kim, Xuan Chen, Yongjie Yang

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

20 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Extracellular Vesicle-Mediated Neuron-Glia Communications in the Central Nervous System.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Review
  10. Review
  11. Review
  12. Molecular hallmarks of ageing in amyotrophic lateral sclerosis.Cellular and molecular life sciences : CMLS · 2024
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. The Evolving Landscape of Motor Neuron Disease Therapeutics.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    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.

Gloria KimDepartment of Neuroscience, Tufts University School of Medicine, 136 Harrison Ave, Boston, MA, 02111, USA.
Xuan ChenDepartment of Neuroscience, Tufts University School of Medicine, 136 Harrison Ave, Boston, MA, 02111, USA.
Yongjie YangDepartment of Neuroscience, Tufts University School of Medicine, 136 Harrison Ave, Boston, MA, 02111, USA. yongjie.yang@tufts.edu.ORCID http://orcid.org/0000-0003-0318-8224
Tufts University · US

Funding

CNS Exosomes-Mediated Adaptive Immunity in Alzheimer's Disease (AD)R01AG078728 · NIA · TUFTS UNIVERSITY BOSTON · PI ALEXEI DEGTEREV, Yongjie Yang · 2022 to 2026
$4.4M
Exosome-mediated propagation of disease linked poly-dipeptides in C9orf72-FTD/ALSRF1AG057882 · NIA · THOMAS JEFFERSON UNIVERSITY · PI TROTTI, DAVIDE, YANG, YONGJIE · 2018 to 2018
$3.6M
Neuronal/Glial exosome signaling and beta-amyloid propagation in Alzheimer's Disease (AD)RF1AG059610 · NIA · TUFTS UNIVERSITY BOSTON · PI TESCO, GIUSEPPINA, YANG, YONGJIE · 2018 to 2018
$2.7M
Exosomal miRNA in neuron to astroglial communication in the CNSR01NS118747 · NINDS · TUFTS UNIVERSITY BOSTON · PI YANG, YONGJIE · 2020 to 2024
$2.2M
Dysfunctional Astroglial Exosome to (motor) Neuron Axon Signaling in ALSR01NS125490 · NINDS · TUFTS UNIVERSITY BOSTON · PI Yongjie Yang · 2022 to 2026
$2.1M
NIA NIH HHS R01 AG078728NIA NIH HHS RF1 AG057882NIA NIH HHS RF1 AG059610NINDS NIH HHS R01 NS118747NINDS NIH HHS R01 NS125490
6 · The paper itself

Abstract

Extracellular vesicles (EVs), once considered a pathway for cells to remove waste, have now emerged as an important mechanism for intercellular communication. EVs are particularly appealing in understanding the central nervous system (CNS) communication, given that there are very diverse cell types in the CNS and constant communications among various cells to respond to the frequently changing environment. While they are heterogeneous and new vesicles are continuously to be discovered, EVs are primarily classified as plasma membrane-derived microvesicles (MVs) and endosome-derived exosomes. Secretion of EVs has been shown from all CNS cell types in vitro and intercellular EV signaling has been implicated in neural development, axon integrity, neuron to glia communication, and propagation of protein aggregates formed by disease pathogenic proteins. However, significant hurdles remain to be tackled in understanding their physiological and pathological roles as well as how they can be developed as biomarkers or new therapeutics. Here we provide our summary on the known cell biology of EVs and discuss opportunities and challenges in understanding EV biology in the CNS and particularly their involvement in ALS pathogenesis.

Indexed as

Amyotrophic Lateral SclerosisExosomesExtracellular VesiclesBiomarkersHumansProtein AggregatesBiomarkersProtein AggregatesALSESCRTEVExosomeNeuron to glia communicationTetraspanin

Identifiers

PMID35426061
PMCPMC9587178
OpenAlexW4223912338

What OpenQuestion holds

Textmetadata
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.