Evidence map›Paper›PMID 28578515›Full record

ArticleMetabolic brain disease2017

Blood assessment of the expression levels of matrix metalloproteinase 9 (MMP9) and its natural inhibitor, TIMP1 genes in Iranian schizophrenic patients.

Shahrzad Rahimi, Arezou Sayad, Elham Moslemi, Soudeh Ghafouri-Fard, Mohammad Taheri

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 26% 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, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Observational
  4. Article
  5. Article
  6. Article
  7. MMPs in learning and memory and neuropsychiatric disorders.Cellular and molecular life sciences : CMLS · 2019
    Review
  8. Article
  9. Article
  10. Article
  11. Upregulation of vitamin D-related genes in schizophrenic patients.Neuropsychiatric disease and treatment · 2018
    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 2 institutions in 1 country.

Shahrzad RahimiDepartment of Biology, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
Arezou SayadDepartment of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, PO Box 1985717443, Tehran, Iran. ar.sayad@yahoo.com.
Elham MoslemiDepartment of Biology, Central Tehran Branch, Islamic Azad University, Tehran, Iran.
Soudeh Ghafouri-FardDepartment of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, PO Box 1985717443, Tehran, Iran.
Mohammad TaheriDepartment of Medical Genetics, School of Medicine, Shahid Beheshti University of Medical Sciences, PO Box 1985717443, Tehran, Iran. Mohammad_823@yahoo.com.
Shahid Beheshti University of Medical Sciences · IRIslamic Azad University Central Tehran Branch · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Schizophrenia (SCZ) is the most severe chronic mental disorder characterized by abnormal social behavior and disrupted emotions and thought. Like other complex neuropsychological disease, SCZ is caused by a combination of genetic and environmental factors but with a high concordance rate. So far, different genetic factors are revealed to be associated with increased risk of developing SCZ. One of the best ways to investigate the genetic basis of the complex disease is to discover the genetic underlying mechanisms of the defective clinical aspects of the patients. In this regard, genes involved in the developmental mechanisms of the brain such as long-term potentiation (LTP) process that is the basis of synaptic plasticity, memory and learning are considered as strong candidates for SCZ. The aim of the present study was to evaluate the expression levels of two genes that are involved in the LTP regulation in the developing and adult brain, Matrix metallopeptidase9 (MMP9) and TIMP metallopeptidase inhibitor 1 (TIMP1) genes in a blood assessment of schizophrenic patients in comparison to healthy controls by means of quantitative real time PCR. The results of the study showed a significant difference in MMP9/TIPM1 ratio between SCZ patients and healthy controls (P = 0.01). However, no significant difference was detected in the expression level of individual MMP9 and TIMP1 genes in SCZ patients versus healthy controls either in total numbers of subject or in sex based subgroups. Considering the relatively small sample size of the current study, there is a need to replicate this study with further investigations about the mechanism of association of these genes and their functions in the pathogenesis of the SCZ.

Indexed as

AdultAgedDNA, ComplementaryFemaleGene ExpressionHumansIranLong-Term PotentiationMaleMatrix Metalloproteinase 9Middle AgedPolymerase Chain ReactionSchizophreniaSchizophrenic PsychologyTissue Inhibitor of Metalloproteinase-1DNA, ComplementaryMatrix Metalloproteinase 9MMP9 protein, humanTIMP1 protein, humanTissue Inhibitor of Metalloproteinase-1Expression analysisMMP9Real time PCRSchizophreniaTIMP1

Identifiers

PMID28578515
OpenAlexW2620760222

What OpenQuestion holds

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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.