Evidence map›Paper›PMID 20064257›Full record

ArticleJournal of biomedical science2010

Genetic copy number variants in sib pairs both affected with schizophrenia.

Chia-Huei Lee, Chih-Min Liu, Chun-Chiang Wen, Shun-Min Chang, Hai-Gwo Hwu

Abstract read
In one paragraph

Article in Journal of biomedical science, 2010. 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
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Psychosis in Alzheimer's disease.Biological psychiatry · 2014
    Review
  10. Genetics of Psychosis in Alzheimer Disease.Current genetic medicine reports · 2014
    Article
  11. Article
  12. Article
  13. Article
  14. 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

5 authors.

Chia-Huei LeeDepartment of Psychiatry, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
Chih-Min Liu
Chun-Chiang Wen
Shun-Min Chang
Hai-Gwo Hwu

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSchizophrenia is a complex disorder with involvement of multiple genes.

methodsIn this study, genome-wide screening for DNA copy-number variations (CNVs) was conducted for ten pairs, a total of 20 cases, of affected siblings using oligonucleotide array-based CGH.

resultsWe found negative symptoms were significantly more severe (p < 0.05) in the subgroup that harbored more genetic imbalance (n >== 13, n = number of CNV-disrupted genes) as compared with the subgroup with fewer CNVs (n <== 6), indicating that the degree of genetic imbalance may influence the severity of the negative symptoms of schizophrenia. Four central nervous system (CNS) related genes including CCAAT/enhancer binding protein, delta (CEBPD, 8q11.21), retinoid x receptor, alpha (RXRA, 9q34.2), LIM homeobox protein 5 (LHX5, 12q24.13) and serine/threonine kinase 11 (STK11, 19p13.3) are recurrently (incidence >== 16.7%) disrupted by CNVs. Two genes, PVR (poliovirus receptor) and BU678720, are concordantly deleted in one and two, respectively, pairs of co-affected siblings. However, we did not find a significant association of this BU678720 deletion and schizophrenia in a large case-control sample.

conclusionsWe conclude that the high genetic loading of CNVs may be the underlying cause of negative symptoms of schizophrenia, and the CNS-related genes revealed by this study warrant further investigation.

Indexed as

AdultComparative Genomic HybridizationDNA Copy Number VariationsGenome, HumanGenome-Wide Association StudyHumansOligonucleotide Array Sequence AnalysisPedigreePolymorphism, Single NucleotideSchizophreniaSiblings

Identifiers

PMID20064257
PMCPMC2843606

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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.