| 1 | Hum. Mol. Genet. 2006 Jun 15: 1949-62 |
|---|---|
| PMID | 16687443 |
| Title | 全基因组检测八个基因表达分析s with robust alterations specific to bipolar I disorder: relevance to neuronal network perturbation. |
| Abstract | The limited number of genome-wide transcriptome analyses using the postmortem brains of bipolar disorder sufferers has not produced a clear consensus on the molecular pathways affected by the disorder. To expand the knowledge in this area, we examined the expression levels of more than 12 000 genes in Brodmann's Area (BA), 46 (dorsolateral prefrontal cortex) from bipolar I disorder and control samples using Affymetrix GeneChips. This analysis detected 108 differentially expressed genes in bipolar brains. Validation studies using quantitative RT-PCR on the two original diagnostic cohorts plus tissue fromschizophrenicsubjects, confirmed the differential expressions of eight genes (RAP1GA1, SST, HLA-DRA, KATNB1, PURA,NDUFV2, STAR and PAFAH1B3) in a bipolar-specific manner and one gene (CCL3) which was downregulated in both bipolar andschizophrenicbrains. Of these, protein levels of RAP1GA1 (RAP1 GTPase activating protein 1) showed a trend of increase in BA46 from bipolar brains, in keeping with mRNA transcript levels. Transmission disequilibrium analysis of the nine genes using 43 single nucleotide polymorphisms (SNPs) in 229 National Institute of Mental Health bipolar trios exposed nominal SNP association and modest empirical haplotypic association (P=0.033) between SST (somatostatin) and disease. Finally, gene network analysis using the currently obtained expression data highlighted cellular growth and nervous system development pathways as potential targets in the molecular pathophysiology of bipolar disorder. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 2 | Am. J. Med. Genet. B Neuropsychiatr. Genet. 2006 Apr 141B: 301-4 |
| PMID | 16508936 |
| Title | Association of mitochondrial complex I subunit gene NDUFV2 at 18p11 with schizophrenia in the Japanese population. |
| Abstract | schizophreniaand bipolar disorder share common genetic background. Several loci such as 18p11, 13q32, and 22q11-13 were commonly linked with these diseases. Since mitochondrial dysfunction has been suggested in both of these disorders,NDUFV2at 18p11, encoding a subunit of the complex I, NADH ubiquinone oxidoreductase, is a candidate gene for these diseases. We previously reported that single nucleotide polymorphisms (SNPs) in the upstream region ofNDUFV2与日语中的躁郁症有关。在日本和国家心理健康研究所三重奏组中，还可以看到由两个SNP组成的单倍型关联，即-3542G> a和-602g> a，以及双相情感障碍。在这项研究中，在229中研究了2种多态性-3542G> a和-602g> aschizophrenic患者与对照组相比。单个基因型与schizophrenia。However, the haplotype consisting of these two SNPs were significantly associated withschizophrenia。These results suggested that inter-individual variation of the genomic sequence of the promoter region ofNDUFV2might be a genetic risk factor common to bipolar disorder andschizophrenia。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 3 | Am. J. Med. Genet. B Neuropsychiatr. Genet. 2006 Apr 141B: 301-4 |
| PMID | 16508936 |
| Title | Association of mitochondrial complex I subunit gene NDUFV2 at 18p11 with schizophrenia in the Japanese population. |
| Abstract | schizophreniaand bipolar disorder share common genetic background. Several loci such as 18p11, 13q32, and 22q11-13 were commonly linked with these diseases. Since mitochondrial dysfunction has been suggested in both of these disorders,NDUFV2at 18p11, encoding a subunit of the complex I, NADH ubiquinone oxidoreductase, is a candidate gene for these diseases. We previously reported that single nucleotide polymorphisms (SNPs) in the upstream region ofNDUFV2与日语中的躁郁症有关。在日本和国家心理健康研究所三重奏组中，还可以看到由两个SNP组成的单倍型关联，即-3542G> a和-602g> a，以及双相情感障碍。在这项研究中，在229中研究了2种多态性-3542G> a和-602g> aschizophrenic患者与对照组相比。单个基因型与schizophrenia。However, the haplotype consisting of these two SNPs were significantly associated withschizophrenia。These results suggested that inter-individual variation of the genomic sequence of the promoter region ofNDUFV2might be a genetic risk factor common to bipolar disorder andschizophrenia。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 4 | Schizophr Bull 2007 Nov 33: 1343-53 |
| PMID | 17329232 |
| Title | eIF2B and oligodendrocyte survival: where nature and nurture meet in bipolar disorder and schizophrenia? |
| Abstract | Bipolar disorder andschizophreniashare common chromosomal susceptibility loci and many risk-promoting genes. Oligodendrocyte cell loss and hypomyelination are common to both diseases. A number of environmental risk factors including famine, viral infection, and prenatal or childhood stress may also predispose toschizophrenia或躁郁症。在细胞中，相关的应激源（饥饿，病毒，细胞因子，氧化和内质网应激）激活一系列EIF2-Alpha激酶，通过磷酸化的EIF2-Alpha，Translation Initization Intiation Intiation initiation initiation initiation initiation initiation initiation启动因子EIF2B，通过最终抑制，通过最终抑制蛋白质合成。生长因子通过EIF2B激活和平衡该系统增加蛋白质的合成。EIF2-Alpha激酶对蛋白质合成的控制也由长期增强参与，并由长期抑郁症抑制，由N-甲基-D-天冬氨酸（NMDA）和代谢型谷氨酸受体介导。据报道，许多基因都与两者相关schizophreniaand bipolar disorder code for proteins within or associated with this network. These include NMDA (GRIN1, GRIN2A, GRIN2B) and metabotropic (GRM3, GRM4) glutamate receptors, growth factors (BDNF, NRG1), and many of their downstream signaling components or accomplices (AKT1, DAO, DAOA, DISC1, DTNBP1, DPYSL2, IMPA2, NCAM1, NOS1, NOS1AP, PIK3C3, PIP5K2A, PDLIM5, RGS4, YWHAH). They also include multiple gene products related to the control of the stress-responsive eIF2-alpha kinases (IL1B, IL1RN, MTHFR, TNF, ND4,NDUFV2, XBP1). Oligodendrocytes are particularly sensitive to defects in the eIF2B complex, mutations in which are responsible for vanishing white matter disease. The convergence of natural and genetic risk factors on this area in bipolar disorder andschizophreniamay help to explain the apparent vulnerability of this cell type in these conditions. This convergence may also help to reconcile certain arguments related to the importance of nature and nurture in the etiology of these psychiatric disorders. Both may affect common stress-related signaling pathways that dictate oligodendrocyte viability and synaptic plasticity. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 5 | PLoS ONE 2007 -1 2: e817 |
| PMID | 17786189 |
| Title | Sp1 expression is disrupted in schizophrenia; a possible mechanism for the abnormal expression of mitochondrial complex I genes, NDUFV1 and NDUFV2. |
| Abstract | The prevailing hypothesis regardsschizophrenia作为一种多基因疾病，其中多个基因相互结合，并与环境刺激相结合，以产生其临床症状的方差。我们研究了无处不在的转录因子SP1是否在schizophrenia, and consequently can affect the expression of genes implicated in this disorder. mRNA of Sp1 and of mitochondrial complex I subunits (NDUFV1,NDUFV2在从斯坦利基金会大脑收集获得的三个验尸大脑区域中分析）schizophrenic患者和对照。还研究了SP1在这些基因转录中的作用。SP1异常表达schizophreniain both brain and periphery. Its mRNA alteration pattern paralleled that of NDUFV1 andNDUFV2, decreasing in the prefrontal cortex and the striatum, while increasing in the parieto-occipital cortex and in lymphocytes ofschizophrenic患者与对照组相比。Moreover, a high and significant correlation between these genes existed in normal subjects, but was distorted in patients. Sp1 role in the regulation of complex I subunits, was demonstrated by the ability of the Sp1/DNA binding inhibitor, mithramycin, to inhibit the transcription of NDUFV1 andNDUFV2, in neuroblastoma cells. In addition, Sp1 activatedNDUFV2promoter by binding to its three GC-boxes. Both activation and binding were inhibited by mithramycin. These findings suggest that abnormality in Sp1, which can be the main activator/repressor or act in combination with additional transcription factors and is subjected to environmental stimuli, can contribute to the polygenic and clinically heterogeneous nature ofschizophrenia。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 6 | PLoS ONE 2007 -1 2: e817 |
| PMID | 17786189 |
| Title | Sp1 expression is disrupted in schizophrenia; a possible mechanism for the abnormal expression of mitochondrial complex I genes, NDUFV1 and NDUFV2. |
| Abstract | The prevailing hypothesis regardsschizophrenia作为一种多基因疾病，其中多个基因相互结合，并与环境刺激相结合，以产生其临床症状的方差。我们研究了无处不在的转录因子SP1是否在schizophrenia, and consequently can affect the expression of genes implicated in this disorder. mRNA of Sp1 and of mitochondrial complex I subunits (NDUFV1,NDUFV2在从斯坦利基金会大脑收集获得的三个验尸大脑区域中分析）schizophrenic患者和对照。还研究了SP1在这些基因转录中的作用。SP1异常表达schizophreniain both brain and periphery. Its mRNA alteration pattern paralleled that of NDUFV1 andNDUFV2, decreasing in the prefrontal cortex and the striatum, while increasing in the parieto-occipital cortex and in lymphocytes ofschizophrenic患者与对照组相比。Moreover, a high and significant correlation between these genes existed in normal subjects, but was distorted in patients. Sp1 role in the regulation of complex I subunits, was demonstrated by the ability of the Sp1/DNA binding inhibitor, mithramycin, to inhibit the transcription of NDUFV1 andNDUFV2, in neuroblastoma cells. In addition, Sp1 activatedNDUFV2promoter by binding to its three GC-boxes. Both activation and binding were inhibited by mithramycin. These findings suggest that abnormality in Sp1, which can be the main activator/repressor or act in combination with additional transcription factors and is subjected to environmental stimuli, can contribute to the polygenic and clinically heterogeneous nature ofschizophrenia。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 7 | PLoS ONE 2008 -1 3: e3676 |
| PMID | 18989376 |
| Title | Neuroanatomical pattern of mitochondrial complex I pathology varies between schizophrenia, bipolar disorder and major depression. |
| Abstract | Mitochondrial dysfunction was reported inschizophrenia, bipolar disorderand major depression. The present study investigated whether mitochondrial complex I abnormalities show disease-specific characteristics. mRNA and protein levels of complex I subunits NDUFV1,NDUFV2and NADUFS1, were assessed in striatal and lateral cerebellar hemisphere postmortem specimens and analyzed together with our previous data from prefrontal and parieto-occipital cortices specimens of patients withschizophrenia, bipolar disorder, major depression and healthy subjects. A disease-specific anatomical pattern in complex I subunits alterations was found.schizophrenia-specific reductions were observed in the prefrontal cortex and in the striatum. The depressed group showed consistent reductions in all three subunits in the cerebellum. The bipolar group, however, showed increased expression in the parieto-occipital cortex, similar to those observed inschizophrenia, and reductions in the cerebellum, yet less consistent than the depressed group. These results suggest that the neuroanatomical pattern of complex I pathology parallels the diversity and similarities in clinical symptoms of these mental disorders. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 8 | J. Proteome Res. 2009 Jul 8: 3633-41 |
| PMID | 19441803 |
| Title | A comparative proteomics analysis of rat mitochondria from the cerebral cortex and hippocampus in response to antipsychotic medications. |
| Abstract | 越来越多的实验发现了心理学大脑中线粒体的异常情况，这表明线粒体功能障碍或脑能量代谢异常可能在病理生理中起重要作用schizophrenia(SCZ). We adopted a proteomic approach to identify the differential effects on the cerebral cortex and hippocampus mitochondrial protein expression of Sprague-Dawley (SD) rats by comparing exposure to typical and atypical antipsychotic medications. Differential mitochondrial protein expressions were assessed using two-dimensional (2D) gel electrophoresis for three groups with Chlorpromazine (CPZ), Clozapine (CLZ), quetiapine (QTP) and a control group. A total of 14 proteins, of which 6 belong to the respiratory electron transport chain (ETC) of oxidative phosphorylation (OXPHOS), showed significant changes in quantity including NADH dehydrogenase (ubiquinone) 1 alpha subcomplex 10 (Ndufa10), NADH dehydrogenase (ubiquinone) flavoprotein 2 (NDUFV2），NADH脱氢酶（Ubiquinone）Fe-S蛋白3（NDUFS3），F1-ATPase Beta亚基（ATP5B），ATPase，H+转运，溶酶体，溶酶体，Beta 56/58 kDa，同4 kDA，等型2（ATP6V1B2）和PPase，h+ Atpase，h+ Atpase，h+运输，v1，v1亚基A，同工型1（ATP6V1A1）。使用定量实时PCR（Q-RT-PCR）评估了遭受2D的差异蛋白的mRNA水平，我们还部分使用了蛋白质印迹来评估差异表达。我们的研究结果可能有助于解释SD大鼠以及人类对抗精神病药的反应的变化。此外，他们应该提高我们对抗精神病药的治疗作用和副作用的理解，并鼓励SCZ研究中的新方向。beplay苹果手机能用吗 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 9 | Neurosci. Res. 2009 Mar 63: 199-204 |
| PMID | 19135101 |
| Title | Expression of mitochondrial complex I subunit gene NDUFV2 in the lymphoblastoid cells derived from patients with bipolar disorder and schizophrenia. |
| Abstract | Several studies have suggested mitochondrial abnormality in bipolar disorder (BD) andschizophrenia(SZ). We have previously reported the decreased expression of mitochondrial complex I subunit gene,NDUFV2at 18p11, in lymphoblastoid cell lines (LCLs) from Japanese patients with bipolar I disorder (BDI). Recently it was reported that no differences were found inNDUFV2mRNA levels in LCLs of Caucasian BDI patients compared with controls. In this study, we tested the altered expression ofNDUFV2in extended Japanese LCLs and LCLs from different ethnic groups. Similar tendency was found in the current study compared with our previous study, since decreased expression ofNDUFV2in LCLs from Japanese patients with BDI was found (p=0.03). We also found that the expressions ofNDUFV2与对照组相比，该基因的日本双极II疾病患者（p = 0.001）的患者被上调（p = 0.001），该基因的mRNA水平下调（p = 0.000001）。此外，我们揭示了mRNA的表达NDUFV2in LCLs cultured with valproate, one of mood stabilizers, were significantly increased compared with controls (p=0.02). Our study presented the further evidence of biological significance ofNDUFV2in BD and SZ. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 10 | Behav Brain Funct 2010 -1 6: 75 |
| PMID | 21190551 |
| Title | Common promoter variants of the NDUFV2 gene do not confer susceptibility to schizophrenia in Han Chinese. |
| Abstract | 通用电气的NADH-ubiquinone氧化还原酶黄素蛋白ne (NDUFV2), which encodes a 24 kD mitochondrial complex I subunit, has been reported to be positively associated withschizophreniaand bipolar disorder in different populations. We genotyped the promoter variants of this gene (rs6506640 and rs1156044) by direct sequencing in 529 unrelated Han Chineseschizophreniapatients and 505 matched controls. Fisher's Exact test was performed to assess whether these two reported single nucleotide polymorphisms (SNPs) confer susceptibility toschizophreniain Chinese. 等位基因、基因型和单体型比较the case and control groups showed no statistical significance, suggesting no association between theNDUFV2gene promoter variants andschizophreniain Han Chinese. The role ofNDUFV2played inschizophrenia需要进一步研究。不同的种族背景和/或人口子结构可能会解释研究之间不一致的结果。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 11 | Parkinsonism Relat. Disord. 2010 Dec 16: 686-7 |
| PMID | 20971673 |
| Title | Genetic variation of the mitochondrial complex I subunit NDUFV2 and Parkinson's disease. |
| Abstract | NADH脱氢酶泛氨酸酮黄素蛋白2（NDUFV2), encoding a subunit of mitochondrial complex I, is a candidate gene for several neuronal diseases;schizophrenia, bipolar disorder and Parkinson disease (PD). We screened the entire coding region ofNDUFV2在33名北非阿拉伯 - 伯伯族的家族性PD患者中，所有已知的PD遗传形式都被排除在外。我们在一个PD概率中检测到了一种新颖的替代P.K209R（C.626a> g）。由于样本量较小，家庭内部的分离分析尚无定论，但与常染色体显性遗传模式一致。随后在种族匹配的零星PD患者（n = 238）和对照组（n = 371）中对该突变进行了筛查，并在另外一名患者中鉴定出P.K209R。突变载体的临床特征显示出一种温和的帕金森氏症形式，预后类似于特发性PD。我们的发现提出了进一步的研究，以解决NDUFV2variation in PD may be warranted. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 12 | J. Biomed. Sci. 2011 -1 18: 29 |
| PMID | 21548921 |
| Title | Mitochondrial targeting of human NADH dehydrogenase (ubiquinone) flavoprotein 2 (NDUFV2) and its association with early-onset hypertrophic cardiomyopathy and encephalopathy. |
| Abstract | NADH dehydrogenase (ubiquinone) flavoprotein 2 (NDUFV2), containing one iron sulfur cluster ([2Fe-2S] binuclear cluster N1a), is one of the core nuclear-encoded subunits existing in human mitochondrial complex I. Defects in this subunit have been associated with Parkinson's disease, Alzheimer's disease, Bipolar disorder, andschizophrenia。The aim of this study is to examine the mitochondrial targeting ofNDUFV2and dissect the pathogenetic mechanism of one human deletion mutation present in patients with early-onset hypertrophic cardiomyopathy and encephalopathy. A series of deletion and point-mutated constructs with the c-myc epitope tag were generated to identify the location and sequence features of mitochondrial targeting sequence forNDUFV2in human cells using the confocal microscopy. In addition, various lengths of theNDUFV2N-terminal and C-terminal fragments were fused with enhanced green fluorescent protein to investigate the minimal region required for correct mitochondrial import. Finally, a deletion construct that mimicked the IVS2+5_+8delGTAA mutation inNDUFV2gene and would eventually produce a shortenedNDUFV2lacking 19-40 residues was generated to explore the connection between human gene mutation and disease. We identified that the cleavage site ofNDUFV2was located around amino acid 32 of the precursor protein, and the first 22 residues ofNDUFV2were enough to function as an efficient mitochondrial targeting sequence to carry the passenger protein into mitochondria. A site-directed mutagenesis study showed that none of the single-point mutations derived from basic, hydroxylated and hydrophobic residues in theNDUFV2presequence had a significant effect on mitochondrial targeting, while increasing number of mutations in basic and hydrophobic residues gradually decreased the mitochondrial import efficacy of the protein. The deletion mutant mimicking the human early-onset hypertrophic cardiomyopathy and encephalopathy lacked 19-40 residues inNDUFV2and exhibited a significant reduction in its mitochondrial targeting ability. The mitochondrial targeting sequence ofNDUFV2is located at the N-terminus of the precursor protein. Maintaining a net positive charge and an amphiphilic structure with the overall balance and distribution of basic and hydrophobic amino acids in the N-terminus ofNDUFV2is important for mitochondrial targeting. The results of human disease cell model established that the impairment of mitochondrial localization ofNDUFV2as a mechanistic basis for early-onset hypertrophic cardiomyopathy and encephalopathy. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 13 | Mol. Psychiatry 2012 Sep 17: 887-905 |
| PMID | 22584867 |
| Title | Convergent functional genomics of schizophrenia: from comprehensive understanding to genetic risk prediction. |
| Abstract | We have used a translational convergent functional genomics (CFG) approach to identify and prioritize genes involved inschizophrenia,能够集成的全基因组association study data with other genetic and gene expression studies in humans and animal models. Using this polyevidence scoring and pathway analyses, we identify top genes (DISC1, TCF4, MBP, MOBP, NCAM1, NRCAM,NDUFV2, RAB18, as well as ADCYAP1, BDNF, CNR1, COMT, DRD2, DTNBP1, GAD1, GRIA1, GRIN2B, HTR2A, NRG1, RELN, SNAP-25, TNIK), brain development, myelination, cell adhesion, glutamate receptor signaling, G-protein-coupled receptor signaling and cAMP-mediated signaling as key to pathophysiology and as targets for therapeutic intervention. Overall, the data are consistent with a model of disrupted connectivity inschizophrenia由于神经发育环境压力对遗传脆弱性的影响而产生。此外，我们展示了如何使用CFG鉴定的顶级候选基因来生成遗传风险预测评分（GRP）以帮助schizophreniadiagnostics, with predictive ability in independent cohorts. The GRPS also differentiates classic age of onsetschizophreniafrom early onset and late-onset disease. We also show, in three independent cohorts, two European American and one African American, increasing overlap, reproducibility and consistency of findings from single-nucleotide polymorphisms to genes, then genes prioritized by CFG, and ultimately at the level of biological pathways and mechanisms. Finally, we compared our top candidate genes forschizophrenia从我们对躁郁症和焦虑症的最高候选基因分析中，我们先前对我们进行的CFG分析以及自闭症和阿尔茨海默氏症领域的发现。总体而言，我们的工作映射了基因组和生物学景观schizophrenia, providing leads towards a better understanding of illness, diagnostics and therapeutics. It also reveals the significant genetic overlap with other major psychiatric disorder domains, suggesting the need for improved nosology. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 14 | ISRN Psychiatry 2013 -1 2013: 620361 |
| PMID | 23738220 |
| Title | Chronic phencyclidine increases synapsin-1 and synaptic adaptation proteins in the medial prefrontal cortex. |
| Abstract | Phencyclidine (PCP) mimics many aspects ofschizophrenia, yet the underlying mechanism of neurochemical adaptation for PCP is unknown. We therefore used proteomics to study changes in the medial prefrontal cortex in animals with PCP-induced behavioural deficits. Male Wistar rats were injected with saline or 5?mg/kg phencyclidine for 5 days followed by two days of washout. Spontaneous alternation behaviour was tested in a Y-maze and then proteins were extracted from the medial prefrontal cortex. 2D-DIGE analysis followed by spot picking and protein identification with mass spectrometry then provided a list of differentially expressed proteins. Treatment with 5?mg/kg phencyclidine decreased the percentage of correct alternations in the Y-maze compared to saline-treated controls. Proteomics analysis of the medial prefrontal cortex found upregulation of 6 proteins (synapsin-1, Dpysl3, Aco2, Fscn1, Tuba1c, and Mapk1) and downregulation of 11 (Bin1, Dpysl2, Sugt1, ApoE, Psme1, ERp29, Pgam1, Uchl1,NDUFV2, Pcmt1, and Vdac1). A trend to upregulation was observed for Gnb4 and Capza2, while downregulation trends were noted for alpha-enolase and Fh. Many of the hits in this study concur with recent postmortem data fromschizophrenic患者及其进一步验证了链勤转移研究中苯基二肽的使用。beplay苹果手机能用吗 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 15 | ISRN Psychiatry 2013 -1 2013: 620361 |
| PMID | 23738220 |
| Title | Chronic phencyclidine increases synapsin-1 and synaptic adaptation proteins in the medial prefrontal cortex. |
| Abstract | Phencyclidine (PCP) mimics many aspects ofschizophrenia, yet the underlying mechanism of neurochemical adaptation for PCP is unknown. We therefore used proteomics to study changes in the medial prefrontal cortex in animals with PCP-induced behavioural deficits. Male Wistar rats were injected with saline or 5?mg/kg phencyclidine for 5 days followed by two days of washout. Spontaneous alternation behaviour was tested in a Y-maze and then proteins were extracted from the medial prefrontal cortex. 2D-DIGE analysis followed by spot picking and protein identification with mass spectrometry then provided a list of differentially expressed proteins. Treatment with 5?mg/kg phencyclidine decreased the percentage of correct alternations in the Y-maze compared to saline-treated controls. Proteomics analysis of the medial prefrontal cortex found upregulation of 6 proteins (synapsin-1, Dpysl3, Aco2, Fscn1, Tuba1c, and Mapk1) and downregulation of 11 (Bin1, Dpysl2, Sugt1, ApoE, Psme1, ERp29, Pgam1, Uchl1,NDUFV2, Pcmt1, and Vdac1). A trend to upregulation was observed for Gnb4 and Capza2, while downregulation trends were noted for alpha-enolase and Fh. Many of the hits in this study concur with recent postmortem data fromschizophrenic患者及其进一步验证了链勤转移研究中苯基二肽的使用。beplay苹果手机能用吗 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 16 | J Mol Psychiatry 2014 -1 2: 6 |
| PMID | 25713723 |
| Title | Mitochondrial complex I and III gene mRNA levels in schizophrenia, and their relationship with clinical features. |
| Abstract | The etiology ofschizophreniais not precisely known; however, mitochondrial function and cerebral energy metabolism abnormalities were determined to be possible factors associated with the etiology ofschizophrenia。Impaired mitochondrial function negatively affects neuronal plasticity, and can cause cognitive deficits and behavioral abnormalities observed during the clinical course ofschizophrenia。本研究旨在研究schizophrenia, and mitochondrial complex activation, based on measurement of mRNA levels in the NDUFV1,NDUFV2, NDUFS1, and UQCR10 genes involved in the peripheral mitochondrial complex. The study included 138schizophreniapatients and 42 healthy controls. Theschizophreniagroup was divided into a chronicschizophreniasubgroup (n?=?84) and a first-episodeschizophrenia子组(n = ? 54)。概要文件和severi症状ty of disorder were evaluated using the Scale for the Assessment of Negative Symptoms (SANS), Scale for the Assessment of Positive Symptoms (SAPS), and Brief Psychiatric Rating Scale (BPRS). The level of mRNA expression of NDUFV1,NDUFV2, and NDUFS1 was significantly higher in theschizophreniagroup than in the control group. The mRNA level ofNDUFV2was positively correlated with BPRS and SAPS scores in the first-episodeschizophreniasubgroup. The findings showed that there was a positive correlation between gene mRNA levels and psychotic symptomatology, especially positive symptoms. Our results suggest that mRNA levels of the NDUFV1, NUDFV2, and NDUFS1 genes of complex I of the mitochondrial electron transport chain might become a possible peripheral marker for the diagnosis ofschizophrenia。 |
| SCZ Keywords | schizophrenia, schizophrenic |
| 17 | Brain Res. 2015 Nov 1625: 102-10 |
| PMID | 26327164 |
| Title | NDUFV2 regulates neuronal migration in the developing cerebral cortex through modulation of the multipolar-bipolar transition. |
| Abstract | Abnormalities during brain development are tightly linked several psychiatric disorders. Mutations in NADH dehydrogenase ubiquinone flavoprotein 2 (NDUFV2）负责schizophrenia, bipolar disorder and Parkinson?s disease. However, the function ofNDUFV2during brain development remains unclear. Here we reported thatNDUFV2is expressed in the developing cerebral cortex. In utero suppression ofNDUFV2arrested neuronal migration, leading to accumulation of ectopic neurons in the intermediate zone.NDUFV2抑制作用不影响径向胶质的支架，祖细胞或神经元存活。但是，损失NDUFV2impairs neuronal multipolar-bipolar transition in vivo and polarization in vitro. Moreover,NDUFV2affected actin cytoskeleton and tubulin stabilization in cortical neurons. Overall, our findings establish a newNDUFV2dependent mechanism underlying neuronal migration and psychiatric disorders. |
| SCZ Keywords | schizophrenia, schizophrenic |
| 18 | J Affect Disord 2016 Jan 190: 329-32 |
| PMID | 26544616 |
| Title | A haplotype in the 5'-upstream region of the NDUFV2 gene is associated with major depressive disorder in Han Chinese. |
| Abstract | 有足够的证据支持这样的想法：线粒体功能障碍和复杂I亚基的表达改变在精神疾病的病理生理学中起重要作用。早期文学报告已牵涉NDUFV2, a nuclear-encoded mitochondrial complex I subunit gene, in bipolar disorder andschizophrenia。There has been no genetic study to investigate whether there is an association betweenNDUFV2and major depressive disorder (MDD). This study recruited 744 patients with MDD and 767 well-matched healthy controls in a Chinese Han population, and genotyped 9 SNPs withinNDUFV2。 Initial analysis showed statistically significant differences for 2 SNPs (rs4798765 and rs12964485) in the genotypic distribution and for 1 SNP (rs4797356) in the allelic distribution between the case and control groups. Nevertheless, no significance was demonstrated following multiple testing corrections. Haplotype analysis showed that the T-C haplotype, consisting of rs12457810 and rs12964485, was significantly associated with MDD (P=0.005, corrected P=0.04 after a 10,000 permutation test). We performed an eQTL analysis and found that rs12964485 was significantly associated withNDUFV2expression in the occipital cortex (P=0.036), albeit this significance did not survive after Bonferroni correction. This is a preliminary investigation with a relatively modest sample size. 我们的发现提供了初步证据，表明由RS12457810和RS12964485组成的单倍型T-C在5'上游区域中NDUFV2may be a protective factor for the development of MDD in Han Chinese. |
| SCZ Keywords | schizophrenia, schizophrenic |