Evidence map›Paper›PMID 39438912›Full record

SynthesisBMC psychiatry2024

Genetic polymorphism involved in major depressive disorder: a systemic review and meta-analysis.

Areeya Suktas, Tipaya Ekalaksananan, Sirinart Aromseree, Sureewan Bumrungthai, Nopparat Songserm, Chamsai Pientong

Abstract readSystematic ReviewMeta-Analysis
In one paragraph

Synthesis in BMC psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
–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 synthesis or guideline pooled it.

  1. Pooled it
  2. Association of the C-1019G (rs6295) Polymorphism of theDiseases (Basel, Switzerland) · 2026
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. 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

6 authors.

Areeya SuktasDepartment of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Tipaya EkalaksanananDepartment of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Sirinart AromsereeDepartment of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand.
Sureewan BumrungthaiFaculty of Pharmaceutical Sciences, Ubon Ratchathani University, Ubon Ratchathani, Thailand.
Nopparat SongsermFaculty of Public Health, Ubon Ratchathani Rajabhat University, Ubon Ratchathani, Thailand.
Chamsai PientongDepartment of Microbiology, Faculty of Medicine, Khon Kaen University, Khon Kaen, Thailand. Chapie@kku.ac.th.

Funding

Faculty of Medicine, Khon Kaen University, Thailand IN66093
6 · The paper itself

Abstract

BACKGROUND AND

objectiveGenetic polymorphism studies in families and twins indicated the heritability of depression. However, the association between genes with genetic polymorphism and depression provides various findings and remains unclear. Therefore, we conducted a systematic review and meta-analysis to determine the genes with their polymorphism associated with the symptomatic depression known as major depressive disorder (MDD). MATERIALS AND

methodsPubMed and Scopus were searched for relevant studies published before May 22, 2023 (1968-2023), and 62 were selected for this review. The study's bias risk was investigated using the Newcastle-Ottawa scale. Gene functional enrichment analysis was investigated for molecular function (MF) and biological process (BP) and pathways. A meta-analysis of the studied genes that were replicative in the same single nucleotide polymorphism was conducted using a random-effect model.

resultsThe 49 genes involved in MDD were studied and engaged in several pathways, such as tryptophan metabolism or dopaminergic and serotonergic synapses. Based on gene overlapping in MF and BP, 13 genes with polymorphisms were identified as related to MDD. Most of them were only studied once. Solute carrier family 6 member 4 (SLC6A4) overlapping between MF and BP and brain-derived neurotrophic factor (BDNF) as unique to BP were replicative studied and used in the meta-analysis. The polymorphism of SLC6A4 SS and LS genotypes increased the occurrence of MDD development but not significantly [odd ratio (OR) = 1.39; 95% confidence interval (CI) = 0.87-2.22; P = 0.16 and OR = 1.13; 95% CI = 0.84-1.53; P = 0.42, respectively]. A similar result was observed for BDNF rs6265 GG (OR = 1.26; 95% CI = 0.78-2.06; P = 0.35) and BDNF rs6265 AA genotypes (OR = 1.12; 95% CI = 0.77-1.64; P = 0.56). These studies indicated low bias and significant heterogeneity.

conclusionAt least 13 studied genes with polymorphisms were involved in MDD development according to MF and BP, but not significantly. These results suggest that MDD development risk factors might require genetic and other factors for interaction and induction.

Indexed as

Major Depressive DisorderBrain-Derived Neurotrophic FactorGenetic Predisposition to DiseaseHumansPolymorphism, Single NucleotideSerotonin Plasma Membrane Transport ProteinsBrain-Derived Neurotrophic FactorSerotonin Plasma Membrane Transport ProteinsSLC6A4 protein, humanBDNFMajor depressive disorderSingle nucleotide polymorphismSLC6A4

Identifiers

PMID39438912
PMCPMC11515766

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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.