ArticleBiological psychiatry2012
Genome-wide linkage analysis of obsessive-compulsive disorder implicates chromosome 1p36.
Article in Biological psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Revealing the complex genetic architecture of obsessive-compulsive disorder using meta-analysis.Molecular psychiatry · 2018Pooled it
- Rare protein-disrupting variants inmedRxiv : the preprint server for health sciences · 2026Article
- Psychiatric Comorbidities in 1p36 Deletion Syndrome and Their Treatment-A Case Report.International journal of environmental research and public health · 2021Article
- Bidirectional Behavioral Selection in Mice: A Novel Pre-clinical Approach to Examining Compulsivity.Frontiers in psychiatry · 2021Review
- Nordic OCD & Related Disorders Consortium: Rationale, design, and methods.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2020Article
- Integrative analysis of shared genetic pathogenesis by autism spectrum disorder and obsessive-compulsive disorder.Bioscience reports · 2019Article
- A Clinical Staging Model for Obsessive-Compulsive Disorder: Is It Ready for Prime Time?EClinicalMedicine · 2019Review
- Biological markers for anxiety disorders, OCD and PTSD: A consensus statement. Part II: Neurochemistry, neurophysiology and neurocognition.The world journal of biological psychiatry : the official journal of the World Federation of Societies of Biological Psychiatry · 2017Review
- Rodent models of obsessive compulsive disorder: Evaluating validity to interpret emerging neurobiology.Neuroscience · 2017Review
- The neurobiological link between OCD and ADHD.Attention deficit and hyperactivity disorders · 2014Review
- Obsessive-compulsive disorder: an integrative genetic and neurobiological perspective.Nature reviews. Neuroscience · 2014Review
- Association between SLC1A1 gene and early-onset OCD in the Han Chinese population: a case-control study.Journal of molecular neuroscience : MN · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
14 authors at 7 institutions in 1 country.
Funding
Abstract
backgroundObsessive-compulsive disorder (OCD) has a complex etiology involving both genetic and environmental factors. However, the genetic causes of OCD are largely unknown, despite the identification of several promising candidate genes and linkage regions.
methodsOur objective was to conduct genetic linkage studies of the type of OCD thought to have the strongest genetic etiology (i.e., childhood-onset OCD), in 33 Caucasian families with ≥2 childhood-onset OCD-affected individuals from the United States (n = 245 individuals with genotype data). Parametric and nonparametric genome-wide linkage analyses were conducted with Morgan and Merlin in these families using a selected panel of single nucleotide repeat polymorphisms from the Illumina 610-Quad Bead Chip. The initial analyses were followed by fine-mapping analyses in genomic regions with initial heterogeneity logarithm of odds (HLOD) scores of ≥2.0.
resultsWe identified five areas of interest (HLOD score ≥2) on chromosomes 1p36, 2p14, 5q13, 6p25, and 10p13. The strongest result was on chromosome 1p36.33-p36.32 (HLOD = 3.77, suggestive evidence for linkage after fine mapping). At this location, several of the families showed haplotypes co-segregating with OCD.
conclusionsThe results of this study represent the strongest linkage finding for OCD in a primary analysis to date and suggest that chromosome 1p36, and possibly several other genomic regions, may harbor susceptibility loci for OCD. Multiple brain-expressed genes lie under the primary linkage peak (approximately 4 megabases in size). Follow-up studies, including replication in additional samples and targeted sequencing of the areas of interest, are needed to confirm these findings and to identify specific OCD risk variants.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.