Evidence map›Paper›PMID 12927051›Full record

ReviewJournal of cellular and molecular medicine

Inflammatory mechanisms associated with brain damage induced by kainic acid with special reference to the interleukin-1 system.

M Oprica, C Eriksson, M Schultzberg

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of cellular and molecular medicine. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed, 1 pooled it
2.4field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Tualang Honey: A Decade of Neurological Research.Molecules (Basel, Switzerland) · 2021
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Honey on brain health: A promising brain booster.Frontiers in aging neuroscience · 2022
    Review
  9. Pretreatment with Methylene Blue Protects Against Acute Seizure and Oxidative Stress in a Kainic Acid-Induced Status Epilepticus Model.Medical science monitor : international medical journal of experimental and clinical research · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Effect of Lead (Pb) on Inflammatory Processes in the Brain.International journal of molecular sciences · 2016
    Review
  16. Immunity and Inflammation in Epilepsy.Cold Spring Harbor perspectives in medicine · 2015
    Review
  17. Review
  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

3 authors at 2 institutions in 1 country.

M OpricaNeurotec Department, Karolinska Institute, Division of Experimental Geriatrics, Huddinge University Hospital, Novum, 4th floor, SE-141 86 Stockholm, Sweden. Mircea.Oprica@neurotec.ki.se
C Eriksson
M Schultzberg
Karolinska University Hospital · SEKarolinska Institutet · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The evidence of inflammatory processes in the clinical manifestations and neuropathological sequelae of epilepsy have accumulated in the last decade. Administration of kainic acid, an analogue of the excitatory amino acid glutamate, induces a characteristic behavioural syndrome and a reproducible pattern of neurodegeneration in several brain areas, closely resembling human temporal lobe epilepsy. Results from studies using the kainic acid model indicate that manipulation of pro- and anti-inflammatory cytokines can modify the outcome with regard to the behavioural syndrome as well as the neuropathological consequences. Interleukin-1 is one of the most important cytokines and has several actions in the brain that are critical for the host defense against injury and infection, and it is involved in the initiation of early stages of inflammation. It is believed that interleukin-1 plays a pivotal role in the neuroinflammation associated with certain forms of neurodegeneration, including cerebral ischemia, trauma and excitotoxic brain injury. In this review, we have summarized the experimental data available with regard to the involvement of the interleukin-1 system in kainic acid-induced changes in the brain and emphasized the modulatory role of interleukin-1beta in this model of epilepsy

Indexed as

AnimalsBrainCaspase 1EpilepsyExcitatory Amino Acid AgonistsGene Expression RegulationHumansInflammationInterleukin-1Kainic AcidNeuroprotective AgentsReceptors, Interleukin-1Signal TransductionCaspase 1Excitatory Amino Acid AgonistsInterleukin-1Kainic AcidNeuroprotective AgentsReceptors, Interleukin-1

Identifiers

PMID12927051
PMCPMC6740282
OpenAlexW1972504460

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.