ArticleMolecular medicine (Cambridge, Mass.)
Analysis of TBX1 variation in patients with psychotic and affective disorders.
Article in Molecular medicine (Cambridge, Mass.). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Chronic D-ribose and D-mannose overload induce depressive/anxiety-like behavior and spatial memory impairment in mice.Translational psychiatry · 2021Article
- Article
- Copy number variation at 22q11.2: from rare variants to common mechanisms of developmental neuropsychiatric disorders.Molecular psychiatry · 2013Review
- 22q11 Gene dosage establishes an adaptive range for sonic hedgehog and retinoic acid signaling during early development.Human molecular genetics · 2013Article
- Cognitive, behavioural and psychiatric phenotype in 22q11.2 deletion syndrome.Behavior genetics · 2011Review
- Short-term selective breeding for high and low prepulse inhibition of the acoustic startle response; pharmacological characterization and QTL mapping in the selected lines.Pharmacology, biochemistry, and behavior · 2008Article
- Top-down or bottom-up: Contrasting perspectives on psychiatric diagnoses.Biologics : targets & therapy · 2008Article
- Schizophrenia and 22q11.2 deletion syndrome.Current psychiatry reports · 2008Review
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10 authors at 4 institutions in 1 country.
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Abstract
A significant portion of patients with 22q11 deletion syndrome (22q11DS) develop psychiatric disorders, including schizophrenia and other psychotic and affective symptoms, and the responsible gene/s are assumed to also play a significant role in the etiology of nonsyndromic psychiatric disease. The most common psychiatric diagnosis among patients with 22q11DS is schizophrenia, thought to result from neurotransmitter imbalances and also from disturbed brain development. Several genes in the 22q11 region with known or suspected roles in neurotransmitter metabolism have been analyzed in patients with isolated schizophrenia; however, their contribution to the disease remains controversial. Haploinsufficiency of the TBX1 gene has been shown to be sufficient to cause the core physical malformations associated with 22q11DS in mice and humans and via abnormal brain development could contribute to 22q11DS-related and isolated psychiatric disease. 22q11DS populations also have increased rates of psychiatric conditions other than schizophrenia, including mood disorders. We therefore analyzed variations at the TBX1 locus in a cohort of 446 white patients with psychiatric disorders relevant to 22q11DS and 436 ethnically matched controls. The main diagnoses included schizophrenia (n = 226), schizoaffective disorder (n = 67), bipolar disorder (n = 82), and major depressive disorder (n = 29). We genotyped nine tag SNPs in this sample but did not observe significant differences in allele or haplotype frequencies in any of the analyzed groups (all affected, schizophrenia and schizoaffective disorder, schizophrenia alone, and bipolar disorder and major depressive disorder) compared with the control group. Based on these results we conclude that TBX1 variation does not make a strong contribution to the genetic etiology of nonsyndromic forms of psychiatric disorders commonly seen in patients with 22q11DS.
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