Search

Introduction: Attention deficit/hyperactivity disorder (ADHD) is a hereditary neurodevelopmental disorder characterized by working memory (WM) deficits. The MnlI variant (rs3746544) of the synaptosomal‐associated protein 25 (SNAP‐25) gene is associated with ADHD. In this study, we investigated the role and underlying mechanism of SNAP‐25 MnlI variant in cognitive impairment and brain functions in boys with ADHD. Method: We performed WM capacity tests using the fourth version of the Wechsler Intelligence Scale for Children (WISC‐IV) and regional homogeneity (ReHo) analysis for the resting‐state functional magnetic resonance imaging data of 56 boys with ADHD divided into two genotypic groups (TT homozygotes and G‐allele carriers). Next, Spearman's rank correlation analysis between the obtained ReHo values and the WM index (WMI) calculated for each participant. Results: Compared with G‐allele carrier group, there were higher ReHo values for the left medial prefrontal cortex (mPFC) and higher WM capacity in TT homozygote group. Contrary to TT homozygote group, the WM capacity was negatively correlated with the peak ReHo value for the left mPFC in G‐allele carrier group. Conclusion: These findings suggest that SNAP‐25 MnlI variant may underlie cognitive and brain function impairments in boys with ADHD, thus suggesting its potential as a new target for ADHD treatment. [ABSTRACT FROM AUTHOR]

Anomalies in large-scale cognitive control networks impacting social attention abilities are hypothesized to be the cause of attention deficit hyperactivity disorder (ADHD). The precise nature of abnormal brain functional connectivity (FC) dynamics including other regions, on the other hand, is unknown. The concept that insular dynamic FC (dFC) among distinct brain regions is dysregulated in children with ADHD was evaluated using Insular subregions, and we studied how these dysregulations lead to social dysfunctioning. Data from 30 children with ADHD and 28 healthy controls (HCs) were evaluated using dynamic resting state functional magnetic resonance imaging (rs-fMRI). We evaluated the dFC within six subdivisions, namely both left and right dorsal anterior insula (dAI), ventral anterior insula (vAI), and posterior insula (PI). Using the insular sub-regions as seeds, we performed group comparison between the two groups. To do so, two sample t -tests were used, followed by post-hoc t -tests. Compared to the HCs, patients with ADHD exhibited decreased dFC values between right dAI and the left middle frontal gyrus, left postcentral gyrus and right of cerebellum crus, respectively. Results also showed a decreased dFC between left dAI and thalamus, left vAI and left precuneus and left PI with temporal pole. From the standpoint of the dynamic functional connectivity of insular subregions, our findings add to the growing body of evidence on brain dysfunction in ADHD. This research adds to our understanding of the neurocognitive mechanisms behind social functioning deficits in ADHD. Future ADHD research could benefit from merging the dFC approach with task-related fMRI and non-invasive brain stimulation, which could aid in the diagnosis and treatment of the disorder. [ABSTRACT FROM AUTHOR]