Evidence map›Paper›PMID 26780491›Full record

ReviewBrain pathology (Zurich, Switzerland)2016

Non-neuronal Cells in ALS: Role of Glial, Immune cells and Blood-CNS Barriers.

Fabiola Puentes, Andrea Malaspina, Johannes M van Noort, Sandra Amor

Open access · greenAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 1 pooled it
9.9field-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

57 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Editorial: Reviews in non-neuronal cells 2024 & 2025.Frontiers in cellular neuroscience · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Causal ALS genes impact the MHC class II antigen presentation pathway.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. 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

4 authors at 1 institution in 2 countries.

Fabiola PuentesNeuroimmunology Unit, Queen Mary University of London, Neuroscience Centre, Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, London, UK.
Andrea MalaspinaNeuroimmunology Unit, Queen Mary University of London, Neuroscience Centre, Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, London, UK.
Johannes M van NoortDelta Crystallon, 2333 CK Leiden, The Netherlands.
Sandra AmorNeuroimmunology Unit, Queen Mary University of London, Neuroscience Centre, Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine and Dentistry, London, UK.
Queen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurological dysfunction and motor neuron degeneration in amyotrophic lateral sclerosis (ALS) is strongly associated with neuroinflammation reflected by activated microglia and astrocytes in the CNS. In ALS endogenous triggers in the CNS such as aggregated protein and misfolded proteins activate a pathogenic response by innate immune cells. However, there is also strong evidence for a neuroprotective immune response in ALS. Emerging evidence also reveals changes in the peripheral adaptive immune responses as well as alterations in the blood brain barrier that may aid traffic of lymphocytes and antibodies into the CNS. Understanding the triggers of neuroinflammation is key to controlling neuronal loss. Here, we review the current knowledge regarding the roles of non-neuronal cells as well as the innate and adaptive immune responses in ALS. Existing ALS animal models, in particular genetic rodent models, are very useful to study the underlying pathogenic mechanisms of motor neuron degeneration. We also discuss the approaches used to target the pathogenic immune responses and boost the neuroprotective immune pathways as novel immunotherapies for ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsBlood-Brain BarrierHumansImmune SystemLymphocytesNeurogliaALSgliaimmune regulationneurodegenerationprotectiontherapy

Identifiers

PMID26780491
PMCPMC8029111
OpenAlexW2257648036

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.