Positive association between synapsin II and schizophrenia

Chen, Qi; He, Guang; Wang, Xiao Yan; Chen, Qing Ying; Liu, Xin Min; Gu, Zhong Zhong; Liu, Jie; Li, Ke Qing; Wang, Shi Ji; Zhu, Shao Ming; Feng, G.; He, Lin

doi:10.1016/j.biopsych.2004.05.010

Cited by 47 publications

(32 citation statements)

References 16 publications

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“…Moreover, several studies showed genetic associations between several CLOCK polymorphisms and SCZ, even though there is not complete consensus as to the specific variants involved [30][31][32][33]. Similarly, several studies showed an association between susceptibility to SCZ and SYN2 [34][35][36] or NRG1 variants [37,38]. However, because of the paucity of studies focusing on these genes and in particular on the specific polymorphisms under investigation in the present study, further research is needed to better explore the existence and the direction of such associations.…”

Section: Discussionmentioning

confidence: 99%

Case–control association study for 10 genes in patients with schizophrenia: influence of 5HTR1A variation rs10042486 on schizophrenia and response to antipsychotics

Crisafulli

Chiesa

Han

et al. 2011

Eur Arch Psychiatry Clin Neurosci

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The aim of this study is to investigate possible associations between a set of single-nucleotide polymorphisms (SNPs) within 10 genes with Schizophrenia (SCZ) and response to antipsychotics in Korean in-patients treated with antipsychotics. Two hundred and twenty-one SCZ in-patients and 170 psychiatrically healthy controls were genotyped for 42 SNPs within ABCB1, ABCB4, TAP2, CLOCK, CPLX1, CPLX2, SYN2, NRG1, 5HTR1A and GPRIN2. Baseline and final clinical measures, including the Positive and Negative Symptoms Scale (PANSS), were recorded. Rs10042486 within 5HTR1A was associated with both SCZ and clinical improvement on PANSS total scores as well as on PANSS positive and PANSS negative scores. The haplotype analyses focusing on the four, three and two blocks' haplotypes within 5HTR1A confirmed such findings as well. We did not observe any significant association between the remaining genetic variants under investigation in this study and clinical outcomes. Our preliminary findings suggest that rs10042486 within 5HTR1A promoter region could be associated with SCZ and with clinical improvement on PANSS total, positive and negative scores in Korean patients with SCZ. However, taking into account the several limitations of our study, further research is needed to draw more definitive conclusions.

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Section: Discussionmentioning

confidence: 99%

Case–control association study for 10 genes in patients with schizophrenia: influence of 5HTR1A variation rs10042486 on schizophrenia and response to antipsychotics

Crisafulli

Chiesa

Han

et al. 2011

Eur Arch Psychiatry Clin Neurosci

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“…Third, behavioural abnormalities are found in the members of the fourgeneration family bearing the SYN1 mutation also in the absence of epilepsy (Garcia et al, 2004). In addition to the behavioural pathology associated with syndromic epilepsy generated by SYN1 mutation, numerous reports found associations between mutations in the human SYN2 gene or SynII expression levels and human schizophrenia (Chen et al, 2004a;Chen et al, 2004b;Grebb and Greengard, 1990;Imai et al, 2001;Mirnics et al, 2000;Saviouk et al, 2007;Vawter et al, 2002) or animals models of schizophrenia (Dyck et al, 2007;Iwazaki et al, 2007). These associations might explain the more-severe behavioural traits displayed by SynII -/-mice during aging and further implicate synapsin mutations in the pathogenesis of neuropsychiatric diseases.…”

Section: Journal Of Cell Science 121 (18)mentioning

confidence: 99%

Synapsin-I- and synapsin-II-null mice display an increased age-dependent cognitive impairment

Corradi¹,

Zanardi

Giacomini³

et al. 2008

Journal of Cell Science

105

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mice during aging. Both SynI-/-and SynII -/-mice displayed behavioural defects that emerged during aging and involved emotional memory in both mutants, and spatial memory in SynII -/-mice. These abnormalities, which were more pronounced in SynII -/-mice, were associated with neuronal loss and gliosis in the cerebral cortex and hippocampus. The data indicate that SynI and SynII have specific and non-redundant functions, and that synaptic dysfunctions associated with synapsin mutations negatively modulate cognitive performances and neuronal survival during senescence.

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“…Vangl2 and Prickle2 also bind and promote postsynaptic clustering of PSD95, critical for maintenance of synaptic integrity [199,227,228]. Prickle1 was found to regulate synaptogenesis and synaptic vesicle trafficking through a direct interaction with synapsin1 (Syn1) [229]; the synapsin protein family have important roles in synapse formation and neurotransmitter release and have previously been implicated in the pathogenesis of psychiatric disorders [230,231,232,233,234,235,236]. Indeed, Prickle1 +/- mice exhibit ASD-like behaviors, and expression of a mutant form of Prickle in cultured cells phenocopies the vesicle trafficking defect observed with aberrant Syn1 function [229].…”

Section: Synapse Formation and Functionmentioning

confidence: 99%

Neurodevelopmental Perspectives on Wnt Signaling in Psychiatry

Mulligan

Cheyette

2016

Complex Psychiatry

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Mounting evidence indicates that Wnt signaling is relevant to pathophysiology of diverse mental illnesses including schizophrenia, bipolar disorder, and autism spectrum disorder. In the 35 years since Wnt ligands were first described, animal studies have richly explored how downstream Wnt signaling pathways affect an array of neurodevelopmental processes and how their disruption can lead to both neurological and behavioral phenotypes. Recently, human induced pluripotent stem cell (hiPSC) models have begun to contribute to this literature while pushing it in increasingly translational directions. Simultaneously, large-scale human genomic studies are providing evidence that sequence variation in Wnt signal pathway genes contributes to pathogenesis in several psychiatric disorders. This article reviews neurodevelopmental and postneurodevelopmental functions of Wnt signaling, highlighting mechanisms, whereby its disruption might contribute to psychiatric illness, and then reviews the most reliable recent genetic evidence supporting that mutations in Wnt pathway genes contribute to psychiatric illness. We are proponents of the notion that studies in animal and hiPSC models informed by the human genetic data combined with the deep knowledge base and tool kits generated over the last several decades of basic neurodevelopmental research will yield near-term tangible advances in neuropsychiatry.

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Positive association between synapsin II and schizophrenia

Cited by 47 publications

References 16 publications

Case–control association study for 10 genes in patients with schizophrenia: influence of 5HTR1A variation rs10042486 on schizophrenia and response to antipsychotics

Case–control association study for 10 genes in patients with schizophrenia: influence of 5HTR1A variation rs10042486 on schizophrenia and response to antipsychotics

Synapsin-I- and synapsin-II-null mice display an increased age-dependent cognitive impairment

Neurodevelopmental Perspectives on Wnt Signaling in Psychiatry

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