Evidence map›Paper›PMID 31168740›Full record

ArticleCell stress & chaperones2019

Regional differences in the inflammatory and heat shock response in glia: implications for ALS.

Benjamin E Clarke, Rebecca San Gil, Jing Yip, Bernadett Kalmar, Linda Greensmith

Abstract read
In one paragraph

Article in Cell stress & chaperones, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Dysregulation of mitochondrial bioenergetics, RNA processing, and cellular stress responses in FUS-ALS: a multi-dataset transcriptomic perspective.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026
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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

5 authors.

Benjamin E ClarkeDepartment of Neuromuscular Diseases, University College London (UCL) Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Rebecca San GilDepartment of Neuromuscular Diseases, University College London (UCL) Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Jing YipDepartment of Neuromuscular Diseases, University College London (UCL) Queen Square Institute of Neurology, London, WC1N 3BG, UK.
Bernadett KalmarDepartment of Neuromuscular Diseases, University College London (UCL) Queen Square Institute of Neurology, London, WC1N 3BG, UK. b.kalmar@ucl.ac.uk.ORCID 0000-0003-3747-4843
Linda GreensmithDepartment of Neuromuscular Diseases, University College London (UCL) Queen Square Institute of Neurology, London, WC1N 3BG, UK.

Funding

Medical Research Council
6 · The paper itself

Abstract

Preferential neuronal vulnerability is characteristic of several neurodegenerative diseases including the motor neuron disease amyotrophic lateral sclerosis (ALS). It is well established that glia play a critical role in ALS, but it is unknown whether regional differences in the ability of glia to support motor neurons contribute to the specific pattern of neuronal degeneration. In this study, using primary mixed glial cultures from different mouse CNS regions (spinal cord and cortex), we examined whether regional differences exist in key glial pathways that contribute to, or protect against, motor neuron degeneration. Specifically, we examined the NF-κB-mediated inflammatory pathway and the cytoprotective heat shock response (HSR). Glial cultures were treated with pro-inflammatory stimuli, tumour necrosis factor-ɑ/lipopolysaccharide or heat stressed to stimulate the inflammatory and HSR respectively. We found that spinal cord glia expressed more iNOS and produced more NO compared to cortical glia in response to inflammatory stimuli. Intriguingly, we found that expression of ALS-causing SOD1

Indexed as

Amyotrophic Lateral SclerosisBrainHeat-Shock ResponseInflammationNeurogliaSpinal CordAnimalsCells, CulturedDisease Models, AnimalHSP70 Heat-Shock ProteinsMiceMice, Inbred C57BLPrimary Cell CultureHSP70 Heat-Shock ProteinsALSAstrogliaHeat shock protein 70Heat shock responseInflammationiNOSMicrogliaNF-κBNO

Identifiers

PMID31168740
PMCPMC6717175

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Registered trials

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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.