A NOS-III haplotype that includes functional polymorphisms is associated with bipolar disorder

Reif, Andreas; Strobel, Alexander; Jacob, Christian; Herterich, Sabine; Freitag, Christine M.; Töpner, T.; Mößner, Rainald; Fritzen, Sabrina; Schmitt, Angelika; Lesch, Klaus‐Peter

doi:10.1017/s1461145705005560

Cited by 35 publications

(31 citation statements)

References 43 publications

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“…We did not include an association analysis with rs2682826, because this SNP does not influence biological function. On the other hand, Reif et al [38] reported an association between the eNOS gene (NOS3) and BP patients. The levels of platelet eNOS activity in MDD patients were lower than in control subjects.…”

Section: Discussionmentioning

confidence: 99%

Genetic Association Analysis of Functional Polymorphisms in Neuronal Nitric Oxide Synthase 1 Gene <i>(NOS1)</i> and Mood Disorders and Fluvoxamine Response in Major Depressive Disorder in the Japanese Population

et al. 2009

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Background/Aim: Nitric oxide has been reported to play a role in neural transmitter release and N-methyl-D-aspartate receptor activation, as well as to be related to oxidative stress. Abnormalities in both of these mechanisms are thought to be involved in the pathophysiology of mood disorders including major depressive disorder (MDD) and bipolar disorder (BP). In addition, several lines of evidence support an association between abnormalities in neuronal nitric oxide synthases (nNOS) and mood disorders. Therefore, we studied the association of nNOS gene (NOS1) and mood disorders and the efficacy of fluvoxamine treatment in Japanese MDD patients. Materials and Methods: Using a single nucleotide polymorphism (SNP; rs41279104, also called ex1c), we conducted a genetic association analysis of case-control samples (325 MDD patients, 154 BP patients and 807 controls) in the Japanese population. In addition, we performed an association analysis between NOS1 and the efficacy of fluvoxamine treatment in 117 MDD patients. We defined a clinical response as a decrease of more than 50% in baseline SIGH-D (Structured Interview Guide for the Hamilton Rating Scale for Depression) score within 8 weeks, and clinical remission as an SIGH-D score of less than 7 at 8 weeks. Results: We did not detect a significant association between NOS1 and MDD, BP or the fluvoxamine therapeutic response in MDD in allele/genotype-wise analysis. Conclusions: We did not detect an association between only one marker (rs41279104) in NOS1 and Japanese mood disorder patients and fluvoxamine response, but sample sizes were probably too small to allow a meaningful test. Moreover, because we did not perform an association analysis based on linkage disequilibrium and a mutation scan of NOS1, a replication of the study using a larger sample and based on linkage disequilibrium may be required for conclusive results.

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Section: Discussionmentioning

confidence: 99%

Genetic Association Analysis of Functional Polymorphisms in Neuronal Nitric Oxide Synthase 1 Gene <i>(NOS1)</i> and Mood Disorders and Fluvoxamine Response in Major Depressive Disorder in the Japanese Population

et al. 2009

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“…Nitrogen retention is dependent upon dietary consumption of nitrogen rich foods along with lipid consumption, electrolyte stability, and mineral density. Analysis of polymorphisms of nitric oxide synthases have not yielded any conclusive evidence for their involvement in the pathogenesis of major depression (Yu et al 2003;Reif et al 2006). In a small sample of 15 subjects with major depression, decreased plasma nitric oxide metabolite levels and platelet endothelial nitric oxide synthase activity were observed (Chrapko et al 2004).…”

Section: Nitrogenmentioning

confidence: 99%

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Mößner

Mikova

Koutsilieri

et al. 2007

The World Journal of Biological Psychiatry

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226

126

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Biological markers for depression are of great interest to aid in elucidating the causes of major depression. We assess currently available biological markers to query their validity for aiding in the diagnosis of major depression. We specifically focus on neurotrophic factors, serotonergic markers, biochemical markers, immunological markers, neuroimaging, neurophysiological findings, and neuropsychological markers. We delineate the most robust biological markers of major depression. These include decreased platelet imipramine binding, decreased 5-HT1A receptor expression, increase of soluble interleukin-2 receptor and interleukin-6 in serum, decreased brain-derived neurotrophic factor in serum, hypocholesterolemia, low blood folate levels, and impaired suppression of the dexamethasone suppression test. To date, however, none of these markers are sufficiently specific to contribute to the diagnosis of major depression. Thus, with regard to new diagnostic manuals such as DSM-V and ICD-11 which are currently assessing whether biological markers may be included in diagnostic criteria, no biological markers for major depression are currently available for inclusion in the diagnostic criteria.

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“…As revealed by immunohistochemical and autoradiographic studies, the distribution of NOS-I achieves its maximum in the cerebellum followed by the hippocampus and neocortex (Bredt and Snyder, 1989 ;Kidd et al, 1995). Another enzyme influencing NO function in the brain is the endothelial nitric oxide synthase (NOS-III) (Reif et al, 2006b). Mice lacking NOS-III show a low rate of neural stem cell proliferation, and in an animal model of depression, i.e.…”

Section: Introductionmentioning

confidence: 99%

Association of functional polymorphisms in NOS1 and NOS3 with loudness dependence of auditory evoked potentials

Kawohl¹,

Giegling²,

Mavrogiorgou³

et al. 2008

Int. J. Neuropsychopharm.

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Nitric oxide (NO) is a gaseous molecule with neurotransmitter properties that is involved in numerous functions in the central nervous system (CNS), the vascular system and also in macrophages. Haplotypes of NOS1 and NOS3 genes have been shown to be associated with different psychiatric disorders such as schizophrenia and bipolar disorder. Therefore, the detection of other characteristics of nitrinergic transmission is desirable. Because nitrinergic functioning influences serotonergic transmission, a functional marker of the serotonergic transmission, the loudness dependence of auditory evoked potentials (LDAEP), can be assumed to be influenced by nitrinergic changes as well. In order to clarify the relationship between nitrinergic transmission and LDAEP, 95 healthy subjects (41 males, 54 females) underwent electrophysiological recording and blood drawing for genotyping of single nucleotide polymorphisms (SNPs) and haplotypes of the NOS1 and NOS3 genes. Interestingly, two functional SNPs in both NOS1 (G-84A_exon 1c promoter polymorphism) and NOS3 (Glu298Asp) were associated with lower LDAEP. Further studies are needed to fully clarify the relationship between nitrinergic transmission, LDAEP and complex disorders such as schizophrenia and affective disorders.

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A NOS-III haplotype that includes functional polymorphisms is associated with bipolar disorder

Cited by 35 publications

References 43 publications

Genetic Association Analysis of Functional Polymorphisms in Neuronal Nitric Oxide Synthase 1 Gene <i>(NOS1)</i> and Mood Disorders and Fluvoxamine Response in Major Depressive Disorder in the Japanese Population

Genetic Association Analysis of Functional Polymorphisms in Neuronal Nitric Oxide Synthase 1 Gene <i>(NOS1)</i> and Mood Disorders and Fluvoxamine Response in Major Depressive Disorder in the Japanese Population

Consensus paper of the WFSBP Task Force on Biological Markers: Biological Markers in Depression

Association of functional polymorphisms in NOS1 and NOS3 with loudness dependence of auditory evoked potentials

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