ArticleFrontiers in neuroscience2016
Meta-Analysis of Tourette Syndrome and Attention Deficit Hyperactivity Disorder Provides Support for a Shared Genetic Basis.
Article in Frontiers in neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 2 of them syntheses that pooled it.
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Who cites it
17 citing papers in PubMed, 2 syntheses or guidelines pooled it, 37 citations in OpenAlex.
- Reconstructing SNP allele and genotype frequencies from GWAS summary statistics.Scientific reports · 2022Pooled it
- Role of Ash1l in Tourette syndrome and other neurodevelopmental disorders.Developmental neurobiology · 2021Pooled it
- Screening Results and Performance of the CBCL Using a two-step Procedure for Mental Disorders in Chinese Children and Adolescents: a five-year Survey.The Psychiatric quarterly · 2025Article
- Neuropsychiatric symptoms in siblings of children with Tourette syndrome in the EMTICS study.JCPP advances · 2025Article
- Article
- Co-Occurrence of Tic Disorders and Attention-Deficit/Hyperactivity Disorder-Does It Reflect a Common Neurobiological Background?Biomedicines · 2022Review
- ADHD and its neurocognitive substrates: A two sample Mendelian randomization study.Translational psychiatry · 2022Article
- The non-essential TSC complex component TBC1D7 restricts tissue mTORC1 signaling and brain and neuron growth.Cell reports · 2022Article
- Transcriptome-wide association study reveals increased neuronal FLT3 expression is associated with Tourette's syndrome.Communications biology · 2022Article
- Comparison of Quantitative Electroencephalography between Tic Disorder and Attention-Deficit/Hyperactivity Disorder in Children.Clinical psychopharmacology and neuroscience : the official scientific journal of the Korean College of Neuropsychopharmacology · 2021Article
- EWAS of Monozygotic Twins Implicate a Role of mTOR Pathway in Pathogenesis of Tic Spectrum Disorder.Genes · 2021Article
- Synaptic processes and immune-related pathways implicated in Tourette syndrome.Translational psychiatry · 2021Article
- Evidence for the placenta-brain axis: multi-omic kernel aggregation predicts intellectual and social impairment in children born extremely preterm.Molecular autism · 2020Article
- Parental Age and Differential Estimates of Risk for Neuropsychiatric Disorders: Findings From the Danish Birth Cohort.Journal of the American Academy of Child and Adolescent Psychiatry · 2019Article
- Polygenic Risk Scores Derived From a Tourette Syndrome Genome-wide Association Study Predict Presence of Tics in the Avon Longitudinal Study of Parents and Children Cohort.Biological psychiatry · 2019Article
- Investigation of previously implicated genetic variants in chronic tic disorders: a transmission disequilibrium test approach.European archives of psychiatry and clinical neuroscience · 2018Article
- Review of the evidence for the management of co-morbid Tic disorders in children and adolescents with attention deficit hyperactivity disorder.World journal of clinical pediatrics · 2018Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Gilles de la Tourette Sydrome (TS) is a childhood onset neurodevelopmental disorder, characterized phenotypically by the presence of multiple motor and vocal tics. It is often accompanied by multiple psychiatric comorbidities, with Attention Deficit/Hyperactivity Disorder (ADHD) among the most common. The extensive co-occurrence of the two disorders suggests a shared genetic background. A major step toward the elucidation of the genetic architecture of TS was undertaken by the first TS Genome-wide Association Study (GWAS) reporting 552 SNPs that were moderately associated with TS (p < 1E-3). Similarly, initial ADHD GWAS attempts and meta-analysis were not able to produce genome-wide significant findings, but have provided insight to the genetic basis of the disorder. Here, we examine the common genetic background of the two neuropsychiatric phenotypes, by meta-analyzing the 552 top hits in the TS GWAS with the results of ADHD first GWASs. We identify 19 significant SNPs, with the top four implicated genes being TBC1D7, GUCY1A3, RAP1GDS1, and CHST11. TBCD17 harbors the top scoring SNP, rs1866863 (p:3.23E-07), located in a regulatory region downstream of the gene, and the third best-scoring SNP, rs2458304 (p:2.54E-06), located within an intron of the gene. Both variants were in linkage disequilibrium with eQTL rs499818, indicating a role in the expression levels of the gene. TBC1D7 is the third subunit of the TSC1/TSC2 complex, an inhibitor of the mTOR signaling pathway, with a central role in cell growth and autophagy. The top genes implicated by our study indicate a complex and intricate interplay between them, warranting further investigation into a possibly shared etiological mechanism for TS and ADHD.
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