Serotonin receptor 1A −1019C/G variant: Impact on antidepressant pharmacoresponse in melancholic depression?
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Acknowledgement
We gratefully acknowledge the skillful technical support of Ms. Kathrin Schwarte.
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Revisiting the behavioral genetics of serotonin: relevance to anxiety and depression
2020, Handbook of Behavioral NeuroscienceCitation Excerpt :There is convincing evidence for a more favorable response to transcranial magnetic stimulation, fluoxetine and various other chemical antidepressants in patients of the 1019C/C genotype (Lemonde, Du, Bakish, Hrdina, & Albert, 2004; Serretti et al., 2004; Yevtushenko, Oros, & Reynolds, 2010; Yu, Tsai, Liou, Hong, & Chen, 2006; Zanardi et al., 2007). However, one recent study did report that carriers of the 1019 C/G genotype demonstrated a poor response to a variety of antidepressant treatments (Baune et al., 2008) and more recently several studies have reported no association with the antidepressant response (Noro et al., 2010; Serretti et al., 2013). Overall, however, it appears that the 1019C/C genotype is associated with a favorable response to antidepressant drugs.
Pharmacogenomics in psychiatric disorders
2018, Pharmacogenomics: Challenges and Opportunities in Therapeutic ImplementationPharmacogenetics in Psychiatry
2018, Advances in PharmacologyDrugs, genes and the blues: Pharmacogenetics of the antidepressant response from mouse to man
2014, Pharmacology Biochemistry and BehaviorCitation Excerpt :Indeed, a more favourable response to various antidepressant treatments including transcranial magnetic stimulation, fluoxetine and other chemical antidepressants has been associated with the 1019C/C genotype (e.g. Lemonde et al., 2004; Serretti et al., 2004a; Yu et al., 2006; Zanardi et al., 2007) although negative findings have also been reported (Illi et al., 2009; Peters et al., 2004). In addition, one study reported that the 1019C/C genotype was associated with a poor rather than a favourable response to a variety of antidepressant treatments (Baune et al., 2008b). The role of a glycine to aspartate substitution at amino acid 272 (rs1800042) in HTR1A in the therapeutic effects of antidepressant drugs has also been investigated.
Pharmacogenetics of Antidepressant Drugs
2014, Handbook of Pharmacogenomics and Stratified MedicinePharmacogenetics in major depression: A comprehensive meta-analysis
2013, Progress in Neuro-Psychopharmacology and Biological PsychiatryCitation Excerpt :Our meta-analysis, that included 1599 subjects more than the previous one focused on HTR1A gene (Zhao et al., 2012a), confirmed no association between rs6295 and AD response or remission. Several studies reported that the G/G genotype or G allele were associated with worse AD efficacy (Arias et al., 2005; Hong et al., 2006; Lemonde et al., 2004; Parsey et al., 2006; Serretti et al., 2004a; Villafuerte et al., 2009; Yu et al., 2006), whereas others reported an opposite association (Baune et al., 2008b; Kato et al., 2009), or no association (Brent et al., 2010; Bukh et al., 2009; Illi et al., 2009; Lin et al., 2009; Noro et al., 2010; Peters et al., 2004; Zhao et al., 2012b). These inconsistent results and the negative findings confirmed by the present review, suggest that rs6295 probably does not play a major role in AD response.