Evidence map›Paper›PMID 31963681›Full record

ReviewJournal of clinical medicine2020

Glial Cells-The Strategic Targets in Amyotrophic Lateral Sclerosis Treatment.

Tereza Filipi, Zuzana Hermanova, Jana Tureckova, Ondrej Vanatko, And Miroslava Anderova

Open access · goldAbstract readReview
In one paragraph

Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.2field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Targeting mitochondrial CaThe Journal of physiology · 2024
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Tanshinone-IIA mediated neuroprotection by modulating neuronal pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
  16. Review
  17. Article
  18. Article
  19. Moderate intrinsic phenotypic alterations inFrontiers in cellular neuroscience · 2023
    Article
  20. Article
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 2 institutions in 1 country.

Tereza FilipiDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, 14200 Prague, Czech Republic.
Zuzana HermanovaDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, 14200 Prague, Czech Republic.
Jana TureckovaDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, 14200 Prague, Czech Republic.
Ondrej VanatkoDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, 14200 Prague, Czech Republic.
And Miroslava AnderovaDepartment of Cellular Neurophysiology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, 14200 Prague, Czech Republic.
Czech Academy of Sciences · CZCzech Academy of Sciences, Institute of Experimental Medicine · CZ

Funding

Grantová Agentura České Republiky 19-02046S
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal neurological disease, which is characterized by the degeneration of motor neurons in the motor cortex and the spinal cord and subsequently by muscle atrophy. To date, numerous gene mutations have been linked to both sporadic and familial ALS, but the effort of many experimental groups to develop a suitable therapy has not, as of yet, proven successful. The original focus was on the degenerating motor neurons, when researchers tried to understand the pathological mechanisms that cause their slow death. However, it was soon discovered that ALS is a complicated and diverse pathology, where not only neurons, but also other cell types, play a crucial role via the so-called non-cell autonomous effect, which strongly deteriorates neuronal conditions. Subsequently, variable glia-based in vitro and in vivo models of ALS were established and used for brand-new experimental and clinical approaches. Such a shift towards glia soon bore its fruit in the form of several clinical studies, which more or less successfully tried to ward the unfavourable prognosis of ALS progression off. In this review, we aimed to summarize current knowledge regarding the involvement of each glial cell type in the progression of ALS, currently available treatments, and to provide an overview of diverse clinical trials covering pharmacological approaches, gene, and cell therapies.

Indexed as

ALSastrocytesclinical trialsmicrogliaNG2-gliaoligodendrocytespericytes

Identifiers

PMID31963681
PMCPMC7020059
OpenAlexW2999194735

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.