Evidence map›Paper›PMID 28127491›Full record

ReviewInternational journal of inflammation2017

Sterile Neuroinflammation and Strategies for Therapeutic Intervention.

Manoj Banjara, Chaitali Ghosh

Abstract readReview
In one paragraph

Review in International journal of inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing 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

54 citing papers in PubMed.

  1. Review
  2. TLC-Derived High-Polar Fractions ofInternational journal of molecular sciences · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. The Neuroimmune System and the Cerebellum.Cerebellum (London, England) · 2024
    Review
  9. Review
  10. Review
  11. Article
  12. Alcohol extract ofBiomedical reports · 2024
    Article
  13. New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Tanshinone-IIA mediated neuroprotection by modulating neuronal pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2023
    Review
  19. Review
  20. 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

2 authors.

Manoj BanjaraCerebrovascular Research, Cleveland Clinic Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0002-6635-7331
Chaitali GhoshCerebrovascular Research, Cleveland Clinic Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Department of Biomedical Engineering, Cleveland Clinic Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Department of Molecular Medicine, Cleveland Clinic Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA.ORCID 0000-0003-4078-0278

Funding

Cytochrome P450-mediated drug interactions at the human blood-brain barrierR01NS095825 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI GHOSH, CHAITALI · 2017 to 2021
$1.7M
Drug brain biotransformation in human refractory epilepsyR01NS078307 · NINDS · CLEVELAND CLINIC LERNER COM-CWRU · PI GHOSH, CHAITALI, MARCHI, NICOLA · 2012 to 2016
$1.7M
NINDS NIH HHS R01 NS078307NINDS NIH HHS R01 NS095825
6 · The paper itself

Abstract

Sterile neuroinflammation is essential for the proper brain development and tissue repair. However, uncontrolled neuroinflammation plays a major role in the pathogenesis of various disease processes. The endogenous intracellular molecules so called damage-associated molecular patterns or alarmins or damage signals that are released by activated or necrotic cells are thought to play a crucial role in initiating an immune response. Sterile inflammatory response that occurs in Alzheimer's disease (AD), Parkinson's disease (PD), stroke, hemorrhage, epilepsy, or traumatic brain injury (TBI) creates a vicious cycle of unrestrained inflammation, driving progressive neurodegeneration. Neuroinflammation is a key mechanism in the progression (e.g., AD and PD) or secondary injury development (e.g., stroke, hemorrhage, stress, and TBI) of multiple brain conditions. Hence, it provides an opportunity for the therapeutic intervention to prevent progressive tissue damage and loss of function. The key for developing anti-neuroinflammatory treatment is to minimize the detrimental and neurotoxic effects of inflammation while promoting the beneficial and neurotropic effects, thereby creating ideal conditions for regeneration and repair. This review outlines how inflammation is involved in the pathogenesis of major nonpathogenic neuroinflammatory conditions and discusses the complex response of glial cells to damage signals. In addition, emerging experimental anti-neuroinflammatory drug treatment strategies are discussed.

Identifiers

PMID28127491
PMCPMC5239986

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.