Evidence map›Paper›PMID 30400801›Full record

ArticleJournal of neuroinflammation2018

Ibuprofen prevents progression of ataxia telangiectasia symptoms in ATM-deficient mice.

Chin Wai Hui, Xuan Song, Fulin Ma, Xuting Shen, Karl Herrup

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

12 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. ATM Kinase-Dependent Regulation of Autophagy: A Key Player in Senescence?Frontiers in cell and developmental biology · 2020
    Review
  9. Article
  10. Review
  11. Accumulation of Cytoplasmic DNA Due to ATM Deficiency Activates the Microglial Viral Response System with Neurotoxic Consequences.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  12. 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

5 authors at 1 institution in 1 country.

Chin Wai HuiDivision of Life Science and State Key Laboratory of Molecular Neurobiology, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Xuan SongDivision of Life Science and State Key Laboratory of Molecular Neurobiology, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Fulin MaDivision of Life Science and State Key Laboratory of Molecular Neurobiology, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Xuting ShenDivision of Life Science and State Key Laboratory of Molecular Neurobiology, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Karl HerrupDivision of Life Science and State Key Laboratory of Molecular Neurobiology, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong. herrup@ust.hk.ORCID http://orcid.org/0000-0001-7786-5844
Hong Kong University of Science and Technology · HK

Funding

The function of ATM protein in the biology of the adult neuron CNS:R01NS071022 · NINDS · RUTGERS, THE STATE UNIV OF N.J. · PI PLUMMER, MARK R. · 2010 to 2014
$2.0M
NINDS NIH HHS R01 NS071022
6 · The paper itself

Abstract

backgroundInflammation plays a critical role in accelerating the progression of neurodegenerative diseases, such as Alzheimer's disease (AD) and ataxia telangiectasia (A-T). In A-T mouse models, LPS-induced neuroinflammation advances the degenerative changes found in cerebellar Purkinje neurons both in vivo and in vitro. In the current study, we ask whether ibuprofen, a non-steroidal anti-inflammatory drug (NSAID), can have the opposite effect and delay the symptoms of the disease.

methodsWe tested the beneficial effects of ibuprofen in both in vitro and in vivo models. Conditioned medium from LPS stimulated primary microglia (LM) applied to cultures of dissociated cortical neurons leads to numerous degenerative changes. Pretreatment of the neurons with ibuprofen, however, blocked this damage. Systemic injection of LPS into either adult wild-type or adult Atm

resultsAdding ibuprofen directly to neuronal cultures significantly reduced LM-induced degeneration. Curiously, adding ibuprofen to the microglia cultures before the LPS challenge had little effect, thus implying a direct effect of the NSAID on the neuronal cultures. In vivo administration of ibuprofen to Atm

conclusionInflammatory processes impact the normal progression of A-T implying that modulation of the immune system can have therapeutic benefit for both the behavioral and cellular symptoms of this neurodegenerative disease.

Indexed as

AnimalsAnimals, NewbornAnti-Inflammatory Agents, Non-SteroidalAtaxia TelangiectasiaAtaxia Telangiectasia Mutated ProteinsCells, CulturedCytokinesDisease Models, AnimalExploratory BehaviorFemaleGene Expression RegulationGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)IbuprofenLipopolysaccharidesMaleMiceAnti-Inflammatory Agents, Non-SteroidalAtaxia Telangiectasia Mutated ProteinsAtm protein, mouseCytokinesGlyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)IbuprofenLipopolysaccharidesNerve Tissue ProteinsAnti-inflammatoryAtaxia telangiectasiaIbuprofenMicrogliaPurkinje cell

Identifiers

PMID30400801
PMCPMC6220455
OpenAlexW2900064344

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.