Variation in the catechol-O-methyltransferase (COMT) gene and treatment response to venlafaxine XR in generalized anxiety disorder

Narasimhan, Sneha; Aquino, Tiffany D.; Multani, Pushpinder Kaur; Rickels, Karl; Lohoff, Falk W.

doi:10.1016/j.psychres.2011.12.034

Cited by 27 publications

(22 citation statements)

References 19 publications

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“…The primary outcome analysis was defined as a reduction of 50% or more in the Hamilton Anxiety Scale (HAM-A) score at 6 months and remission with a HAM-A score of 7 or below. The secondary outcome measurement was the Clinical Global Impression of Improvement (CGI-I) score, with improvement defined as a CGI-I of 1 and 2 [54–56]. Overall, no significant association between the primary outcome measure and the rs4680 variant (Val158Met) in the COMT gene could be established in the 112 European-American patients of this cohort [54].…”

Section: Pharmacogenomicsmentioning

confidence: 99%

“…The secondary outcome measurement was the Clinical Global Impression of Improvement (CGI-I) score, with improvement defined as a CGI-I of 1 and 2 [54–56]. Overall, no significant association between the primary outcome measure and the rs4680 variant (Val158Met) in the COMT gene could be established in the 112 European-American patients of this cohort [54]. However, a slight dominant effect of the A-allele (Met) compared with the G allele (Val) is shown when the CGI-I scale is used as secondary outcome measure [54].…”

Section: Pharmacogenomicsmentioning

confidence: 99%

“…Overall, no significant association between the primary outcome measure and the rs4680 variant (Val158Met) in the COMT gene could be established in the 112 European-American patients of this cohort [54]. However, a slight dominant effect of the A-allele (Met) compared with the G allele (Val) is shown when the CGI-I scale is used as secondary outcome measure [54]. In the same cohort of 156 anxious patients, a trend of association was found for the HTR2A rs7997012 G allele with a difference in frequency between responders (70%) and nonresponders (56%) at 6 months ( P =0.05) using the HAM-A score as described above [55].…”

Section: Pharmacogenomicsmentioning

confidence: 99%

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Sangkuhl¹,

Stingl

Turpeinen

et al. 2014

Pharmacogenetics and Genomics

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Section: Pharmacogenomicsmentioning

confidence: 99%

Section: Pharmacogenomicsmentioning

confidence: 99%

Section: Pharmacogenomicsmentioning

confidence: 99%

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Sangkuhl¹,

Stingl

Turpeinen

et al. 2014

Pharmacogenetics and Genomics

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“…Tetrapods exhibit one type of bone tissue, but they have three types of cartilage: elastic cartilage, hyaline cartilage, and fibrocartilage [6,23,24]. Here, we focus on the predominant type of cartilage in vertebrates, hyaline cartilage, which serves as the template for bone during endochondral ossification.…”

Section: Introductionmentioning

confidence: 99%

“…Collagens are the most abundant proteinaceous skeletal matrix components, and tetrapod chondrocytes and osteoblasts typically express different fibrillar collagens. In tetrapods, Collagen type 1 alpha 2 (Col1a2) is expressed abundantly in bone and is absent from cartilage, while Collagen type 2 alpha 1 (Col2a1) typifies cartilage and is not expressed in tetrapod bone [23,24]. Hyaline cartilage chondrocytes undergo a maturation process during development, when they express Collagen type 10 alpha 1 (Col10a1), but tetrapod bone does not express Col10a1 [15,25].…”

Section: Introductionmentioning

confidence: 99%

Evolution of the osteoblast: skeletogenesis in gar and zebrafish

et al. 2012

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BackgroundAlthough the vertebrate skeleton arose in the sea 500 million years ago, our understanding of the molecular fingerprints of chondrocytes and osteoblasts may be biased because it is informed mainly by research on land animals. In fact, the molecular fingerprint of teleost osteoblasts differs in key ways from that of tetrapods, but we do not know the origin of these novel gene functions. They either arose as neofunctionalization events after the teleost genome duplication (TGD), or they represent preserved ancestral functions that pre-date the TGD. Here, we provide evolutionary perspective to the molecular fingerprints of skeletal cells and assess the role of genome duplication in generating novel gene functions. We compared the molecular fingerprints of skeletogenic cells in two ray-finned fish: zebrafish (Danio rerio)--a teleost--and the spotted gar (Lepisosteus oculatus)--a "living fossil" representative of a lineage that diverged from the teleost lineage prior to the TGD (i.e., the teleost sister group). We analyzed developing embryos for expression of the structural collagen genes col1a2, col2a1, col10a1, and col11a2 in well-formed cartilage and bone, and studied expression of skeletal regulators, including the transcription factor genes sox9 and runx2, during mesenchymal condensation.ResultsResults provided no evidence for the evolution of novel functions among gene duplicates in zebrafish compared to the gar outgroup, but our findings shed light on the evolution of the osteoblast. Zebrafish and gar chondrocytes both expressed col10a1 as they matured, but both species' osteoblasts also expressed col10a1, which tetrapod osteoblasts do not express. This novel finding, along with sox9 and col2a1 expression in developing osteoblasts of both zebrafish and gar, demonstrates that osteoblasts of both a teleost and a basally diverging ray-fin fish express components of the supposed chondrocyte molecular fingerprint.ConclusionsOur surprising finding that the "chondrogenic" transcription factor sox9 is expressed in developing osteoblasts of both zebrafish and gar can help explain the expression of chondrocyte genes in osteoblasts of ray-finned fish. More broadly, our data suggest that the molecular fingerprint of the osteoblast, which largely is constrained among land animals, was not fixed during early vertebrate evolution.

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Association analysis between the A118G polymorphism in the OPRM1 gene and treatment response to venlafaxine XR in generalized anxiety disorder

Cooper

Rickels

Lohoff

2013

Human Psychopharmacology

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Patients diagnosed with generalized anxiety disorder (GAD) exhibit differential responses to standard antidepressant pharmacotherapy. Mounting evidence demonstrates that genetic differences may be implicated in treatment response in disorders like GAD. In this study, we examined whether the OPRM1 gene, which has been implicated in antidepressant treatment response in major depressive disorder, also has an effect in GAD. In our study, 156 patients diagnosed with GAD received venlafaxine XR treatment as part of an 18-month relapse prevention study. Genotypes were obtained for the OPRM1 functional variant A118G for the entire sample (n = 151); however, only the European American population was considered (n = 108) for pharmacogenetic analysis. We found no significant association between A118G and antidepressant treatment response in our GAD population. Future studies that include different single nucleotide polymorphisms of the OPRM1 gene as well as larger populations will need to be conducted to further elucidate the pharmacogenetic role of the endogenous opioid system in anxiety disorders.

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Variation in the catechol-O-methyltransferase (COMT) gene and treatment response to venlafaxine XR in generalized anxiety disorder

Cited by 27 publications

References 19 publications

PharmGKB summary

PharmGKB summary

Evolution of the osteoblast: skeletogenesis in gar and zebrafish

Association analysis between the A118G polymorphism in the OPRM1 gene and treatment response to venlafaxine XR in generalized anxiety disorder

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