ArticleAmerican journal of human genetics2005
Assessment of the effect of age at onset on linkage to bipolar disorder: evidence on chromosomes 18p and 21q.
Article in American journal of human genetics, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 49 citations in OpenAlex.
- Genome-wide association study of early-onset bipolar I disorder in the Han Taiwanese population.Translational psychiatry · 2021Pooled it
- The genetics of early-onset bipolar disorder: A systematic review.Journal of affective disorders · 2015Pooled it
- Clinical correlates of age at onset distribution in bipolar disorder: a comparison between diagnostic subgroups.International journal of bipolar disorders · 2017Article
- Review of the genetic basis of emotion dysregulation in children and adolescents.World journal of psychiatry · 2015Review
- A non-parametric approach for detecting gene-gene interactions associated with age-at-onset outcomes.BMC genetics · 2014Article
- Genomic view of bipolar disorder revealed by whole genome sequencing in a genetic isolate.PLoS genetics · 2014Article
- A variable age of onset segregation model for linkage analysis, with correction for ascertainment, applied to glioma.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2012Article
- Genome-wide association analysis of age at onset and psychotic symptoms in bipolar disorder.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2011Article
- A genome-wide linkage study of bipolar disorder and co-morbid migraine: replication of migraine linkage on chromosome 4q24, and suggestion of an overlapping susceptibility region for both disorders on chromosome 20p11.Journal of affective disorders · 2010Article
- Article
- Two complex genotypes relevant to the kynurenine pathway and melanotropin function show association with schizophrenia and bipolar disorder.Schizophrenia research · 2009Article
- Positive association of the pericentrin (PCNT) gene with major depressive disorder in the Japanese population.Journal of psychiatry & neuroscience : JPN · 2009Article
- The genetics of bipolar disorder: genome 'hot regions,' genes, new potential candidates and future directions.Molecular psychiatry · 2008Review
- Genetics of bipolar disorder.Current psychiatry reports · 2007Review
- Dense SNP association study for bipolar I disorder on chromosome 18p11 suggests two loci with excess paternal transmission.Molecular psychiatry · 2007Article
- Genetic determination in onset age of wrist fracture.Journal of human genetics · 2007Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Previous evidence suggests that the inheritance of bipolar disorder (BP) may vary depending on the age at onset (AAO). Therefore, we sought to incorporate AAO as a covariate in linkage analyses of BP using two different methods, LODPAL and ordered-subset analysis (OSA), in genomewide scans of 150 multiplex pedigrees with 874 individuals. The LODPAL analysis identified two loci, on chromosomes 21q22.13 (LOD = 3.29; empirical chromosomewide P value = .009) and 18p11.2 (LOD = 2.83; empirical chromosomewide P = .05), with increased linkage among subjects who had early onset (AAO < or = 21 years) and later onset (AAO >21 years), respectively. The finding on 21q22.13 was significant at the chromosomewide level, even after correction for multiple testing. Moreover, a similar finding was observed in an independent sample of 65 pedigrees (LOD = 2.88; empirical chromosomewide P = .025). The finding on 18p11.2 was only nominally significant and was not observed in the independent sample. However, 18p11.2 emerged as one of the strongest regions in the OSA (LOD = 2.92; empirical P = .001), in which it was the only finding to meet chromosomewide levels of significance after correction for multiple testing. These results suggest that 21q22.13 and 18p11.2 may harbor genes that increase the risks for early-onset and later-onset forms of BP, respectively. There have been previous reports of linkage on 21q22.13 and 18p11.2, but the findings have not been consistent. This inconsistency may be due to differences in the AAO characteristics of the samples examined. Future studies to fine map susceptibility genes for BP on chromosomes 21q22.13 and 18p11.2 should take AAO into account.
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