Evidence map›Paper›PMID 33583639›Full record

ReviewHuman immunology2021

The role of immune-mediated alterations and disorders in ALS disease.

João Rodrigues Lima-Junior, David Sulzer, Cecilia S Lindestam Arlehamn, Alessandro Sette

Open access · hybridAbstract readReview
In one paragraph

Review in Human immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.5field-weighted citation impact, top 9% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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  12. Mis-spliced transcripts generatebioRxiv : the preprint server for biology · 2023
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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 2 institutions in 1 country.

João Rodrigues Lima-JuniorLa Jolla Institute for Immunology, Center for Autoimmunity and Inflammation, La Jolla, CA 92037, USA.
David SulzerDepartment of Neurology, Columbia University; New York State Psychiatric Institute, New York, NY 10032, USA; Departments of Psychiatry and Pharmacology, Columbia University; New York State Psychiatric Institute, New York, NY 10032, USA.
Cecilia S Lindestam ArlehamnLa Jolla Institute for Immunology, Center for Autoimmunity and Inflammation, La Jolla, CA 92037, USA.
Alessandro SetteLa Jolla Institute for Immunology, Center for Autoimmunity and Inflammation, La Jolla, CA 92037, USA; Department of Medicine, University of California San Diego, La Jolla, CA 92093, USA. Electronic address: alex@lji.org.
La Jolla Institute for Immunology · USColumbia University · US

Funding

Autoimmune Features of Neurodegenerative DisordersR01NS095435 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI SETTE, ALESSANDRO, SULZER, DAVID · 2018 to 2022
$4.2M
NINDS NIH HHS R01 NS095435
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder that leads to neuronal death in the brain and spinal cord. Over the last decades, evidence has emerged regarding the functional diversity of astrocytes, microglia, and T cells in the central nervous system (CNS), and the role of neuroinflammation in ALS. In this review, we summarize current knowledge regarding neuroinflammation in ALS, both at the level of specific molecular pathways and potential cellular pathways as well as outline questions about the immune mechanisms involved in ALS pathogenesis.

Indexed as

Amyotrophic Lateral SclerosisAnimalsAutoimmunityBrainHumansImmunity, CellularNeurogenic InflammationNeurogliaNeuronsSignal TransductionSpinal CordT-LymphocytesALSAutoimmunityGlial cellsNeuroinflammation

Identifiers

PMID33583639
PMCPMC7942756
OpenAlexW3129758780

What OpenQuestion holds

Textmetadata
LicenceTDM
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.