The SCAN-3:C and SCAN-3:A test batteries were used to assess auditory processing abilities; Lucid Ability test for NVIQ; Children's Communication Checklist-2 (CCC-2) for language ability; Swanson Nolan and Pelham-IV Rating Scale (SNAP-IV) for ADHD; and the manual dexterity components of the Movement Assessment Battery for Children-2 (MABC-2) as a screening tool for DCD.
Rhythmicity of finger tapping (P = 0.008) and performance on the dexterity (P = 0.007) and aiming and catching (P = 0.042) components of the MABC-2 were also significantly poorer in the ADHD group than controls.
Once other variables such as age, gender, SES, and ADHD symptomatology were taken into account, the only BRIEF-P subscale that was associated with the MABC-2 Total Score was the Working Memory subscale.
In sum, ADHD and OCD patients showed mostly disorder-specific patterns of brain abnormalities in both task positive salience/ventral attention networks with lateral frontal deficits in ADHD and middle ACC deficits in OCD, as well as in their deactivation patterns in medial frontal DMN regions.
G protein-coupled receptor kinase-interacting protein-1 (GIT1) has recently been reported to be associated with ADHD in human and the genetic deletion of GIT1 result in ADHD-like behaviors in mice.
Recently, a Korean group assessed the G-protein-coupled receptor kinase-interacting protein 1 (GIT1) gene that had previously been associated with ADHD.
The G protein-coupled receptor kinase interacting protein 1 gene (<i>GIT1</i>) has been proposed to be a risk gene for attention deficit hyperactivity disorder (ADHD), and it regulates the endocytosis of G protein-coupled receptors like dopamine receptors.
We found that SNPs within the LPHN3 gene interact with SNPs spanning the 11q region that contains DRD2 and NCAM1 not only to increase the risk of developing ADHD but also to increase ADHD severity.
As we have identified that common variants of the LPHN3 gene were responsible for the 4q linkage signal, we focused on 4q-11q interaction to determine that single-nucleotide polymorphisms (SNPs) harbored in the LPHN3 gene interact with SNPs spanning the 11q region that contains DRD2 and NCAM1 genes, to double the risk of developing ADHD.
Interestingly, the 4q13.1 linkage peak (lod 2.34) occurred immediately upstream of the LPHN3 gene, recently reported both linked and associated with ADHD.
The results of our study further strengthen the concept of an LPHN3 risk haplotype for ADHD and support the usefulness of the endophenotype approach in psychiatric and psychological research.
Linkage and replicated association of ADHD with a novel non-candidate gene (LPHN3) provide new insights into the genetics, neurobiology, and treatment of ADHD.