A possible association between the [minus sign]116C/G single nucleotide polymorphism of the XBP1 gene and lithium prophylaxis in bipolar disorder

Masui, Takuya; Hashimoto, Ryota; Kusumi, Ichiro; Suzuki, Kaoru; Tanaka, Teruaki; Nakagawa, Shin; Kunugi, Hiroshi; Koyama, Tsukasa

doi:10.1017/s1461145705005523

Cited by 50 publications

(24 citation statements)

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“…The period of observation was 2 years. The same lack of association was found in the same year by Masui et al [59] in a sample of 83 bipolar I and 78 bipolar II patients, all of Japanese origins. The period of observation was 1 year in that case.…”

Section: Challenging the Chronic Molecular Events: Results From Pharmsupporting

confidence: 81%

Pharmacogenetics of Lithium Long-Term Treatment: Focus on Initiation and Adaptation Mechanisms

Serretti

Drago

2010

Neuropsychobiology

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Bipolar disorder is a common disease with a high impact in terms of personal suffering and socioeconomic burden. The disentanglement of the molecular deregulations that cause this disorder is pivotal to the understanding of its etiology. This will hopefully cast the engineering of new and more favorable treatments. New insights in the molecular aspects of bipolar disorder may be brought by the understanding of the pharmacodynamics of lithium, the first-line treatment for this disease. The mechanisms by which lithium exerts its activity in the central nervous system are not fully clarified: it is hypothesized that lithium may drive acute molecular events whose activation over time triggers long-lasting modifications in critical neuronal nets. These events are associated with long-lasting changes in the expression profile of genes in neurons that are embedded in these crucial nets. The molecular events that are acutely and chronically triggered by lithium will be reviewed here and matched with the evidence that arises from the pharmacogenetics investigations. Moreover, the pharmacogenetics reports that are not strictly associated with the mechanisms that are thought to be acutely and chronically elicited by lithium will be included in the final part of the paper.

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Section: Challenging the Chronic Molecular Events: Results From Pharmsupporting

confidence: 81%

Pharmacogenetics of Lithium Long-Term Treatment: Focus on Initiation and Adaptation Mechanisms

Serretti

Drago

2010

Neuropsychobiology

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“…Pharmacogenomic studies that aimed to identify genetic variants associated with lithium treatment responses, efficacy, tolerability, and safety in patients with BPD have identified novel SNPs located in protein coding genes. Candidate gene studies have reported several polymorphisms associated with lithium treatment response located in the 5-HTT [101,102], [74], and CACNG2 [103] genes (see Table 2). …”

Section: Lithium Treatment For Bipolar Disordermentioning

confidence: 99%

“…Encodes a protein that catalyzes the decarboxylation of aspartate, cysteine sulfinic acid, and cysteic acid to beta-alanine, hypotaurine, and taurine, respectively [74,90] Two linked SNPs, rs17026688 and rs17026651 mapped to GADL1 gene showed associations with lithium response in patients with BPD [17] pharmacogenomics studies of mood disorders are described below. They can be considered as future opportunities for pharmacogenomic studies in mood disorders.…”

Section: Inositol Polyphosphate-1--phosphatasementioning

confidence: 99%

Pharmacogenomics in the treatment of mood disorders: Strategies and Opportunities for personalized psychiatry

2017

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Personalized medicine (personalized psychiatry in a specific setting) is a new model towards individualized care, in which knowledge from genomics and other omic pillars (microbiome, epigenomes, proteome, and metabolome) will be combined with clinical data to guide efforts to new drug development and targeted prescription of the existing treatment options. In this review, we summarize pharmacogenomic studies in mood disorders that may lay the foundation towards personalized psychiatry. In addition, we have discussed the possible strategies to integrate data from omic pillars as a future path to personalized psychiatry. So far, the progress of uncovering single nucleotide polymorphisms (SNPs) underpinning treatment efficacy in mood disorders (e.g., SNPs associated with selective serotonin re-uptake inhibitors or lithium treatment response in patients with bipolar disorder and major depressive disorder) are encouraging, but not adequate. Genetic studies have pointed to a number of SNPs located at candidate genes that possibly influence response to; (a) antidepressants COMT, HTR2A, HTR1A, CNR1, SLC6A4, NPY, MAOA, IL1B, GRIK4, BDNF, GNB3, FKBP5, CYP2D6, CYP2C19, and ABCB1 and (b) mood stabilizers (lithium) 5-HTT, TPH, DRD1, FYN, INPP1, CREB1, BDNF, GSK3β, ARNTL, TIM, DPB, NR3C1, BCR, XBP1, and CACNG2. We suggest three alternative and complementary strategies to implement knowledge gained from pharmacogenomic studies. The first strategy can be to implement diagnostic, therapeutic, or prognostic genetic testing based on candidate genes or gene products. The second alternative is an integrative analysis (systems genomics approach) to combine omics data obtained from the different pillars of omics investigation, including genomics, epigenomes, proteomics, metabolomics and microbiomes. The main goal of system genomics is an identification and understanding of biological pathways, networks, and modules underlying drug-response. The third strategy aims to the development of multivariable diagnostic or prognostic algorithms (tools) combining individual's genomic information (polygenic score) with other predictors (e.g., omics pillars, neuroimaging, and clinical characteristics) to finally predict therapeutic outcomes. An integration of molecular science with that of traditional clinical practice is the way forward to drug discoveries and novel therapeutic approaches and to characterize psychiatric disorders leading to a better predictive, preventive, and personalized medicine (PPPM) in psychiatry. With future advances in the omics technology and methodological developments for data integration, the goal of PPPM in psychiatry is promising.

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“…-116C>G NA 66 Japanese [Masui, et al 2005] Significant mtDNA 10398A>G rs2853826 54 Japanese [Washizuka, et al 2003]…”

Section: Tph1mentioning

confidence: 99%

Pharmacogenetics in Affective Disorders: A Drug Response Approach

Lefebvre¹,

Del-Favero

2006

CPG

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Affective disorders, including unipolar (UP) disorder and bipolar (BP) disorder are among the most important causes of death and disability worldwide and result in high costs in terms of morbidity as well as mortality. Although the etiology and pathophysiology is widely unknown, family-, twin-and adoption studies argue for a strong genetic determination of these disorders.These studies indicate that there is between 40-85% heritability for these disorders but point also to the importance of environmental factors. Despite the availability of a wide range of different drugs, about 30-50% of patients do not respond properly to acute treatment.Here we provide an overview of genetic drug response markers for affective disorder. Central in review is the question if individual therapeutic outcome for a given treatment can be predicted using genetic markers? An overview of pharmacogenetic and pharmacogenomic approaches is described for selective serotonin reuptake inhibitors (SSRIs), tricyclic antidepressants (TCAs), and mood stabilizing drugs in relation to each of the major candidate genes for affective disorders.

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A possible association between the [minus sign]116C/G single nucleotide polymorphism of the XBP1 gene and lithium prophylaxis in bipolar disorder

Cited by 50 publications

References 0 publications

Pharmacogenetics of Lithium Long-Term Treatment: Focus on Initiation and Adaptation Mechanisms

Pharmacogenetics of Lithium Long-Term Treatment: Focus on Initiation and Adaptation Mechanisms

Pharmacogenomics in the treatment of mood disorders: Strategies and Opportunities for personalized psychiatry

Pharmacogenetics in Affective Disorders: A Drug Response Approach

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