ArticleBiological psychiatry2013
The impact of copy number deletions on general cognitive ability and ventricle size in patients with schizophrenia and healthy control subjects.
Article in Biological psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.
- Genetic copy number variants, cognition and psychosis: a meta-analysis and a family study.Molecular psychiatry · 2021Pooled it
- Variation in fourteen brain structure volumes in schizophrenia: A comprehensive meta-analysis of 246 studies.Neuroscience and biobehavioral reviews · 2019Pooled it
- Copy Number Variations in Neuropsychiatric Disorders.International journal of molecular sciences · 2023Review
- A review of the cognitive impact of neurodevelopmental and neuropsychiatric associated copy number variants.Translational psychiatry · 2023Review
- The contribution of copy number variants to psychiatric symptoms and cognitive ability.Molecular psychiatry · 2023Review
- Treatment resistant schizophrenia: Clinical, biological, and therapeutic perspectives.Neurobiology of disease · 2019Review
- Genetic influences on cognitive endophenotypes in schizophrenia.Schizophrenia research · 2014Article
- Complex rare variation and its role in endophenotypic variation in schizophrenia.Biological psychiatry · 2013Article
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14 authors at 6 institutions in 2 countries.
Funding
Abstract
backgroundGeneral cognitive ability is usually lower in individuals with schizophrenia, partly due to genetic influences. However, the specific genetic features related to general cognitive ability are poorly understood. Individual variation in a specific type of mutation, uncommon genetic deletions, has recently been linked with both general cognitive ability and risk for schizophrenia.
methodsWe derived measures of the aggregate number of "uncommon" deletions (i.e., those occurring in 3% or less of our combined samples) and the total number of base pairs affected by these deletions in individuals with schizophrenia (n = 79) and healthy control subjects (n = 110) and related each measure to the first principal component of a large battery of cognitive tests, a common technique for characterizing general cognitive ability. These two measures of mutation load were also evaluated for relationships with total brain gray matter, white matter, and lateral ventricle volume.
resultsThe groups did not differ on genetic variables. Multivariate general linear models revealed a group (control subjects vs. patients) × uncommon deletion number interaction, such that the latter variable was associated with lower general cognitive ability and larger ventricles in patients but not control subjects.
conclusionsThese data suggest that aggregate uncommon deletion burden moderates central features of the schizophrenia phenotype.
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