Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9952964 | Biological Psychology | 2018 | 25 Pages |
Abstract
Attention deficit/hyperactivity disorder (ADHD) is a highly heritable neurodevelopment disorder. The deficit in working memory is a central cognitive impairment in ADHD. The SNAP-25 is a neurotransmitter vesicular docking protein whose MnlI polymorphism (rs3746544) is located in the 3â²-untranslated region (3â²-UTR) and known to be linked to ADHD, but the underlying mechanism of this polymorphism remains unclear. Using a functional connectivity density (FCD) mapping method based on resting-state functional magnetic resonance imaging in a sample of male children diagnosed with ADHD, we first investigated the correlation between SNAP-25 rs3746544 and FCD hubs. Compared with rs3746544 G-allele carriers, TT homozygous, which confers a high risk for ADHD, exhibited significantly decreased local and long-range FCD in anterior cingulate cortex, and decreased local FCD in the dorsal lateral prefrontal cortex. Moreover, both higher local and long-range FCD could predict better WM capacity. The current findings provide new insights into the underlying neural mechanisms linking SNAP-25 rs3746544 with the risk for ADHD via the endophenotype of brain functional connectivity.
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Authors
Chao Wang, Binrang Yang, Diangang Fang, Hongwu Zeng, Xiaowen Chen, Gang Peng, Qiuying Cheng, Guohua Liang,