Evidence map›Paper›PMID 24677591›Full record

ArticleAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2014

Glycogen synthase kinase 3 beta gene structural variants as possible risk factors of bipolar depression.

Zsolt Ronai, Reka Kovacs-Nagy, Eszter Szantai, Zsuzsanna Elek, Maria Sasvari-Szekely, Gabor Faludi, Judit Benkovits, Janos M Rethelyi, Anna Szekely

Abstract read
In one paragraph

Article in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Epigenetic Modifications of Major Depressive Disorder.International journal of molecular sciences · 2016
    Review
  10. Article
  11. Review
  12. Genomic structural variation in affective, anxiety, and stress-related disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2015
    Review
  13. Article
  14. 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

9 authors at 2 institutions in 1 country.

Zsolt RonaiInstitute of Medical Chemistry, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest, Hungary.
Reka Kovacs-Nagy
Eszter Szantai
Zsuzsanna Elek
Maria Sasvari-Szekely
Gabor Faludi
Judit Benkovits
Janos M Rethelyi
Anna Szekely
Semmelweis University · HUEötvös Loránd University · HU

Funding

The Serotonergic System and Self- or Other-Damaging BehaviorsR03TW007656 · FIC · SEMMELWEIS UNIVERSITY · PI SASVARI-SZEKELY, MARIA · 2007 to 2009
$102k
FIC NIH HHS R03 TW007656
6 · The paper itself

Abstract

The glycogen synthase kinase 3B (GSK3B) is an important target protein of several antidepressants, such as lithium, a mood stabilizer. Recent studies associated structural variations of the GSK3B gene to bipolar disorder (BP), although replications were not conclusive. Here we present data on copy number variations (CNVs) of the GSK3B gene probing the 9th exon region in 846 individuals (414 controls, 172 patients with major depressive disorder (MDD) and 260 with BP). A significant accumulation (odds ratio: 5.5, P = 0.00051) of the amplified exon 9 region was found in patients (22 out of 432) compared to controls (4 of 414). Analyzing patient subgroups, GSK3B structural variants were found to be risk factors of BP particularly (P = 0.00001) with an odds ratio of 8.1 while no such effect was shown in the MDD group. The highest odds (19.7 ratio) for bipolar disorder was observed in females with the amplified exon 9 region. A more detailed analysis of the identified GSK3B CNV by a set of probes covering the GSK3B gene and the adjacent NR1I2 and C3orf15 genes showed that the amplified sequences contained 3' (downstream) segments of the GSK3B and NR1I2 genes but none of them involved the C3orf15 gene. Therefore, the copy number variation of the GSK3B gene could be described as a complex set of structural variants involving partial duplications and deletions, simultaneously. In summary, here we confirmed significant association of the GSK3B CNV and bipolar disorder pointing out that the copy number and extension of the CNV varies among individuals.

Indexed as

Genetic Predisposition to DiseaseAdolescentAdultAgedBipolar DisorderDNA Copy Number VariationsFemaleGenotypeGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaHumansMaleMiddle AgedPolymorphism, Single NucleotideRisk FactorsYoung AdultGlycogen Synthase Kinase 3Glycogen Synthase Kinase 3 betaGSK3B protein, humanbipolar depressioncopy number variationglycogen synthase kinase 3 betaGSK3Bmajor depressionstructural variants

Identifiers

PMID24677591
PMCPMC3980030
OpenAlexW2063003502

What OpenQuestion holds

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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.