The impact of SNAP25 on brain functional connectivity density and working memory in ADHD

Wang, Chao; Yang, Binrang; Fang, Diangang; Zeng, Hongwu; Chen, Xiaowen; Peng, Gang; Cheng, Qing; Liang, Guohua

doi:10.1016/j.biopsycho.2018.08.005

Cited by 22 publications

(19 citation statements)

References 48 publications

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“…1 ). This particular result seems to be consistent with the literature quoted above concerning the pathophysiological role of SNAP-25 (Braida et al 2015 ; Houenou et al 2017 ; Wang et al 2018 ). However, it was surprising to find a very significant increase in the expression of the Snap25 gene in the hippocampus and cerebellum in both experimental groups (Figs.…”

Section: Discussionsupporting

confidence: 93%

“…Below the histograms are presented photos of the full length of blots showing the content of SNAP-25 and β-actin. On these exemplary blots, each group is represented by material from three different male animals consistent with the literature quoted above concerning the pathophysiological role of SNAP-25 (Braida et al 2015;Houenou et al 2017;Wang et al 2018). However, it was surprising to find a very significant increase in the expression of the Snap25 gene in the hippocampus and cerebellum in both experimental groups (Figs.…”

Section: Discussionmentioning

confidence: 94%

“…Genetic studies confirmed the association of Snap25 with ADHD, schizophrenia, and major depressive disorder (Houenou et al 2017 ; Wang et al 2018 ; Wang et al 2015 ); however, apart from the report on the relationship between the Snap25 polymorphism and ASD in the Iranian population (Safari et al 2017 ), the direct association between SNAP-25 and ASD has never been shown in humans. Nevertheless, SNAP-25 is known to play a role in cognitive functions and regulation of locomotor activity, and consequently, associations of this protein with cognitive disorders and hyperactivity have been demonstrated (Guerini et al 2011 ; Karmakar et al 2018 ; Wang et al 2018 ). Other genetic studies investigating autistic children, supported by experiments using the heterozygous Snap-25 (±) mouse model, have shown a significant association of the Snap25 polymorphism with reduced cognitive scores in ASD and indicated that the reduced expression of Snap25 could be responsible for the cognitive deficit (Braida et al 2015 ; Braida et al 2016 ).…”

Section: Discussionmentioning

confidence: 97%

“…More specifically, it has been hypothesized that the Snap25 polymorphism can be assigned roles in the sex-associated differences in behavioral deficits of patients with ADHD and ASD (Ghezzo et al 2009). Genetic studies confirmed the association of Snap25 with ADHD, schizophrenia, and major depressive disorder (Houenou et al 2017;Wang et al 2018;Wang et al 2015); however, apart from the report on the relationship between the Snap25 polymorphism and ASD in the Iranian population (Safari et al 2017), the direct association between SNAP-25 and ASD has never been shown in humans. Nevertheless, SNAP-25 is known to play a role in cognitive functions and regulation of locomotor activity, and consequently, associations of this protein with cognitive disorders and hyperactivity have been demonstrated (Guerini et al 2011;Karmakar et al 2018;Wang et al 2018).…”

Section: Discussionmentioning

confidence: 99%

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Changes in the Expression of SNAP-25 Protein in the Brain of Juvenile Rats in Two Models of Autism

et al. 2020

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The results of genetic studies suggest a possible role for SNAP-25 polymorphism in the development of autism spectrum disorders (ASDs); however, there are no data available on whether changes in SNAP-25 expression also affect animals in rodent models of ASD. The aim of the present study was to explore this issue. The studies included 1-month-old rats representing valproic acid (VPA)-and thalidomide (THAL)-induced models of autism. Their mothers received single doses of VPA (800 mg/kg) or THAL (500 mg/kg) per os on the 11th day of gestation. SNAP-25 protein content in the cerebellum, hippocampus, and frontal lobe was determined using Western blotting, while changes of mRNA levels of Snap25 gene were determined using real-time polymerase chain reaction. Compared to controls, SNAP-25 content was decreased by approximately 35% in all brain structures tested, in both males and females, exclusively in the VPA group. In contrast to this, Snap25 expression, studied in males, was increased in the hippocampus and cerebellum in both, VPA-and THAL-treated rats. We discuss the compliance of these results with the hypothesized role of SNAP-25 in the pathophysiology of ASD and the adequacy of the experimental models used.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

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Changes in the Expression of SNAP-25 Protein in the Brain of Juvenile Rats in Two Models of Autism

et al. 2020

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“…It is known that the synaptosomal-associated protein 25 (SNAP25), together with syntaxin-1A (STX1A) and vesicle-associated membrane protein 2 (VAMP2), mediates neurotransmitters released by the fusion of synaptic vesicles [162,163]. It was also already reported that alterations in gene expression of SNAP25 in mammals are associated with schizophrenia-like behavior [164], and sequence variations in the SNAP25 locus are associated with attention-deficit/hyperactivity disorder (ADHD) [165][166][167].…”

Section: Synaptic Vesicle Trafficking and Exocytosismentioning

confidence: 99%

Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective

Barros

Leão

Santis

et al. 2021

ncRNA

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Non-syndromic intellectual disability (NS-ID or idiopathic) is a complex neurodevelopmental disorder that represents a global health issue. Although many efforts have been made to characterize it and distinguish it from syndromic intellectual disability (S-ID), the highly heterogeneous aspect of this disorder makes it difficult to understand its etiology. Long noncoding RNAs (lncRNAs) comprise a large group of transcripts that can act through various mechanisms and be involved in important neurodevelopmental processes. In this sense, comprehending the roles they play in this intricate context is a valuable way of getting new insights about how NS-ID can arise and develop. In this review, we attempt to bring together knowledge available in the literature about lncRNAs involved with molecular and cellular pathways already described in intellectual disability and neural function, to better understand their relevance in NS-ID and the regulatory complexity of this disorder.

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

et al. 2022

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Introduction Attention deficit/hyperactivity disorder (ADHD) is a hereditary neurodevelopmental disorder characterized by working memory (WM) deficits. The Mnl I 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 Mnl I 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 Mnl I 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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The impact of SNAP25 on brain functional connectivity density and working memory in ADHD

Cited by 22 publications

References 48 publications

Changes in the Expression of SNAP-25 Protein in the Brain of Juvenile Rats in Two Models of Autism

Changes in the Expression of SNAP-25 Protein in the Brain of Juvenile Rats in Two Models of Autism

Non-Syndromic Intellectual Disability and Its Pathways: A Long Noncoding RNA Perspective

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

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