ArticleJournal of psychiatric research2008
Investigation of the G protein subunit Galphaolf gene (GNAL) in attention deficit/hyperactivity disorder.
Article in Journal of psychiatric research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- A preliminary investigation of the differences in immune responses in different strains of mice with localized allergic rhinitis tolerance models.The World Allergy Organization journal · 2025Article
- Two novel genomic regions associated with fearfulness in dogs overlap human neuropsychiatric loci.Translational psychiatry · 2019Article
- Olfactory Receptors in Non-Chemosensory Organs: The Nervous System in Health and Disease.Frontiers in aging neuroscience · 2016Review
- Expanding the toolbox of ADHD genetics. How can we make sense of parent of origin effects in ADHD and related behavioral phenotypes?Behavioral and brain functions : BBF · 2015Review
- Genetics in dystonia: an update.Current neurology and neuroscience reports · 2013Review
- The genetics of dystonia: new twists in an old tale.Brain : a journal of neurology · 2013Review
- Mutations in GNAL cause primary torsion dystonia.Nature genetics · 2013Article
- Parent-of-origin effects of FAS and PDLIM1 in attention-deficit/hyperactivity disorder.Journal of psychiatry & neuroscience : JPN · 2012Article
- Epigenetics in Developmental Disorder: ADHD and Endophenotypes.Journal of genetic syndromes & gene therapy · 2011Article
- Normal gut microbiota modulates brain development and behavior.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Identification of a specific assembly of the g protein golf as a critical and regulated module of dopamine and adenosine-activated cAMP pathways in the striatum.Frontiers in neuroanatomy · 2011Article
- On genome-wide association studies for family-based designs: an integrative analysis approach combining ascertained family samples with unselected controls.American journal of human genetics · 2010Article
- The spontaneously hypertensive rat model of ADHD--the importance of selecting the appropriate reference strain.Neuropharmacology · 2009Review
- A comparison of molecular alterations in environmental and genetic rat models of ADHD: a pilot study.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2008Article
- No preferential transmission of paternal alleles at risk genes in attention-deficit hyperactivity disorder.Molecular psychiatry · 2007Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The dopamine system plays an important role in the regulation of attention and motor behavior, subsequently, several dopamine-related genes have been associated with Attention Deficit/Hyperactivity Disorder (ADHD). Among them are the dopamine receptors D1 and D5 that mediate adenylyl cyclase activation through coupling with G(s)-like proteins. We thus hypothesized that the G(s)-like subunit Galpha(olf), expressed in D1-rich areas of the brain, contributes to the genetic susceptibility of ADHD. To evaluate the involvement of the Galpha(olf) gene, GNAL, in ADHD, we examined the inheritance pattern of 12 GNAL polymorphisms in 258 nuclear families ascertained through a proband with ADHD (311 affected children) using the transmission/disequilibrium test (TDT). Categorical analysis of individual marker alleles demonstrated biased transmission of one polymorphism in GNAL intron 3 (rs2161961; P=0.011). We also observed significant relationships between rs2161961 and dimensional symptoms of inattention and hyperactivity/impulsivity (P=0.003 and P=0.008). In addition, because of recent evidence of imprinting at the GNAL locus, secondary analyses were split into maternal and paternal transmissions to assess a contribution of parental effects. We found evidence of strong maternal effect, with preferential transmission of maternal alleles for rs2161961A (P=0.005) and rs8098539A (P=0.035). These preliminary findings suggest a possible contribution of GNAL in the susceptibility to ADHD, with possible involvement of parent-of-origin effects.
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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.