ArticlePloS one2014
An inherited small microdeletion at 15q13.3 in a patient with early-onset obsessive-compulsive disorder.
Article in PloS one, 2014. 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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Who cites it
9 citing papers in PubMed, 78 citations in OpenAlex.
- Redox-Driven Epigenetic Modifications in Sperm: Unraveling Paternal Influences on Embryo Development and Transgenerational Health.Antioxidants (Basel, Switzerland) · 2025Review
- Article
- Genetics of obsessive-compulsive disorder.Psychological medicine · 2021Review
- Formins in Human Disease.Cells · 2021Review
- Initial findings of striatum tripartite model in OCD brain samples based on transcriptome analysis.Scientific reports · 2019Article
- High resolution chromosomal microarray analysis in paediatric obsessive-compulsive disorder.BMC medical genomics · 2017Article
- High resolution analysis of rare copy number variants in patients with autism spectrum disorder from Taiwan.Scientific reports · 2017Article
- Article
- Whole-exome sequencing in obsessive-compulsive disorder identifies rare mutations in immunological and neurodevelopmental pathways.Translational psychiatry · 2016Article
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
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Abstract
Copy number variations (CNVs) have been previously associated with several different neurodevelopmental psychiatric disorders, such as autism, schizophrenia, and attention deficit hyperactivity disorder (ADHD). The present study consisted of a pilot genome-wide screen for CNVs in a cohort of 16 patients with early-onset obsessive-compulsive disorder (OCD) and 12 mentally healthy individuals, using array-based comparative genomic hybridization (aCGH) on 44K arrays. A small rare paternal inherited microdeletion (∼64 kb) was identified in chromosome 15q13.3 of one male patient with very early onset OCD. The father did not have OCD. The deletion encompassed part of the FMN1 gene, which is involved with the glutamatergic system. This finding supports the hypothesis of a complex network of several genes expressed in the brain contributing for the genetic risk of OCD, and also supports the glutamatergic involvement in OCD, which has been previously reported in the literature.
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