Evidence map›Paper›PMID 29314569›Full record

ArticleJournal of cellular and molecular medicine2018

Association between single nucleotide polymorphisms of TPH1 and TPH2 genes, and depressive disorders.

Paulina Wigner, Piotr Czarny, Ewelina Synowiec, Michał Bijak, Katarzyna Białek, Monika Talarowska, Piotr Galecki, Janusz Szemraj, Tomasz Sliwinski

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 32 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 3 pooled it
1.9field-weighted citation impact, top 15% 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

32 citing papers in PubMed, 3 syntheses or guidelines pooled it, 58 citations in OpenAlex.

  1. Pooled it
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  8. Decoding serotonin: the molecular symphony behind depression.Frontiers in cellular neuroscience · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Paulina WignerLaboratory of Medical Genetics, Department of Molecular Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
Piotr CzarnyDepartment of Medical Biochemistry, Medical University of Lodz, Lodz, Poland.
Ewelina SynowiecLaboratory of Medical Genetics, Department of Molecular Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
Michał BijakDepartment of General Biochemistry, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
Katarzyna BiałekLaboratory of Medical Genetics, Department of Molecular Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.
Monika TalarowskaDepartment of Adult Psychiatry, Medical University of Lodz, Lodz, Poland.
Piotr GaleckiDepartment of Adult Psychiatry, Medical University of Lodz, Lodz, Poland.
Janusz SzemrajDepartment of Medical Biochemistry, Medical University of Lodz, Lodz, Poland.
Tomasz SliwinskiLaboratory of Medical Genetics, Department of Molecular Genetics, Faculty of Biology and Environmental Protection, University of Lodz, Lodz, Poland.ORCID 0000-0001-8385-7744
University of Łódź · PLMedical University of Lodz · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tryptophan catabolites pathway disorders are observed in patients with depression. Moreover, single nucleotide polymorphisms of tryptophan hydroxylase genes may modulate the risk of depression occurrence. The objective of our study was to confirm the association between the presence of polymorphic variants of TPH1 and TPH2 genes, and the development of depressive disorders. Six polymorphisms were selected: c.804-7C>A (rs10488682), c.-1668T>A (rs623580), c.803+221C>A (rs1800532), c.-173A>T (rs1799913)-TPH1, c.-1449C>A (rs7963803), and c.-844G>T (rs4570625)-TPH2. A total of 510 DNA samples (230 controls and 280 patients) were genotyped using TaqMan probes. Among the studied polymoorphisms, the G/G genotype and G allele of c.804-7C>A-TPH1, the T/T homozygote of c.803+221C>A-TPH1, the A/A genotype and A allele of c.1668T>A-TPH1, the G/G homozygote and G allele of c.-844G>T-TPH2, and the C/A heterozygote and A allele of c.-1449C>A-TPH2 were associated with the occurrence of depression. However, the T/T homozygote of c.-1668T>A-TPH1, the G/T heterozygote and T allele of c.-844G>T-TPH2, and the C/C homozygote and C allele of c.-1449C>A-TPH2 decreased the risk of development of depressive disorders. Each of the studied polymorphisms modulated the risk of depression for selected genotypes and alleles. These results support the hypothesis regarding the involvement of the pathway in the pathogenesis of depression.

Indexed as

Polymorphism, Single NucleotideAdultAgedAllelesDepressive DisorderFemaleGene FrequencyGenetic Predisposition to DiseaseGenotypeHumansMaleMiddle AgedRisk FactorsTryptophan HydroxylaseTPH1 protein, humanTPH2 protein, humanTryptophan Hydroxylasedepressionsingle nucleotide polymorphismtryptophan catabolites pathwaystryptophan hydroxylase

Identifiers

PMID29314569
PMCPMC5824396
OpenAlexW2783385666

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.