Role of SNAP‐25 MnlI variant in impaired working memory and brain functions in attention deficit/hyperactivity disorder

Abstract 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 investigat...

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發表在:Brain and Behavior
Main Authors: Diangang Fang, Binrang Yang, Peng Wang, Tong Mo, Yungen Gan, Guohua Liang, Rong Huang, Hongwu Zeng
格式: Article
語言:英语
出版: Wiley 2022-10-01
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在線閱讀:https://doi.org/10.1002/brb3.2758
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author Diangang Fang
Binrang Yang
Peng Wang
Tong Mo
Yungen Gan
Guohua Liang
Rong Huang
Hongwu Zeng
author_facet Diangang Fang
Binrang Yang
Peng Wang
Tong Mo
Yungen Gan
Guohua Liang
Rong Huang
Hongwu Zeng
author_sort Diangang Fang
collection DOAJ
container_title Brain and Behavior
description Abstract 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.
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spelling doaj-art-c878d571cf2b4f04b06b3bbc2ac8a2ac2025-08-19T21:28:58ZengWileyBrain and Behavior2162-32792022-10-011210n/an/a10.1002/brb3.2758Role of SNAP‐25 MnlI variant in impaired working memory and brain functions in attention deficit/hyperactivity disorderDiangang Fang0Binrang Yang1Peng Wang2Tong Mo3Yungen Gan4Guohua Liang5Rong Huang6Hongwu Zeng7Department of Radiology Shenzhen Children's Hospital Shenzhen ChinaDevelopment and Behavior Specialty Shenzhen Children's Hospital Shenzhen ChinaCardiac Rehabilitation Center Fuwai Hospital CAMS&PUMC Beijing ChinaDepartment of Radiology Shenzhen Children's Hospital Shenzhen ChinaDepartment of Radiology Shenzhen Children's Hospital Shenzhen ChinaDepartment of Radiology Shenzhen Children's Hospital Shenzhen ChinaDepartment of Radiology Peking University Shenzhen hospital Shenzhen ChinaDepartment of Radiology Shenzhen Children's Hospital Shenzhen ChinaAbstract 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.https://doi.org/10.1002/brb3.2758ADHDbrain functionSNAP‐25working memory
spellingShingle Diangang Fang
Binrang Yang
Peng Wang
Tong Mo
Yungen Gan
Guohua Liang
Rong Huang
Hongwu Zeng
Role of SNAP‐25 MnlI variant in impaired working memory and brain functions in attention deficit/hyperactivity disorder
ADHD
brain function
SNAP‐25
working memory
title Role of SNAP‐25 MnlI variant in impaired working memory and brain functions in attention deficit/hyperactivity disorder
title_full Role of SNAP‐25 MnlI variant in impaired working memory and brain functions in attention deficit/hyperactivity disorder
title_fullStr Role of SNAP‐25 MnlI variant in impaired working memory and brain functions in attention deficit/hyperactivity disorder
title_full_unstemmed Role of SNAP‐25 MnlI variant in impaired working memory and brain functions in attention deficit/hyperactivity disorder
title_short Role of SNAP‐25 MnlI variant in impaired working memory and brain functions in attention deficit/hyperactivity disorder
title_sort role of snap 25 mnli variant in impaired working memory and brain functions in attention deficit hyperactivity disorder
topic ADHD
brain function
SNAP‐25
working memory
url https://doi.org/10.1002/brb3.2758
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