The Experts below are selected from a list of 324 Experts worldwide ranked by ideXlab platform
Enrico Smeraldi - One of the best experts on this subject based on the ideXlab platform.
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SSRIs Antidepressant Activity is influenced by Gβ3 variants
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2003Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Cristina Lorenzi, Enrico Lattuada, Adele Pirovano, Marco Catalano, Enrico SmeraldiAbstract:Abstract The aim of the present study was to test a possible effect of the G-protein β3-subunit (Gβ3) C825T gene variant on the Antidepressant Activity of selective serotonin reuptake inhibitors (SSRIs) in a sample of major and bipolar depressives, with or without psychotic features. Four hundred and ninety inpatients were treated with fluvoxamine 300 mg/day ( n =362) or paroxetine 40 mg/day ( n =128) and either placebo or pindolol in a double-blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. Gβ3 allelic variants were determined in each subject using a PCR-based technique. Subjects with Gβ3 T/T variants showed better response to treatment ( P =0.009) and this effect was independent from analyzed demographic and clinical variables. These results confirm preliminary reports and shed further light on the genetics of the response to Antidepressant treatments.
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Influence of monoamine oxidase A and serotonin receptor 2A polymorphisms in SSRI Antidepressant Activity
The international journal of neuropsychopharmacology, 2002Co-Authors: Cristina Cusin, Raffaella Zanardi, David Rossini, Roberta Lilli, Alessandro Serretti, Cristina Lorenzi, Enrico Lattuada, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the monoamine oxidase A (MAOA) and serotonin receptor 2A (5-HT-2A) gene variants on the Antidepressant Activity of fluvoxamine and paroxetine in a sample of major (n = 248) and bipolar (n = 195) depressives, with or without psychotic features. A total of 443 in-patients were treated with 300 mg fluvoxamine (n = 307) or 20-40 mg paroxetine (n = 136) for 6 wk. The severity of depressive symptoms was assessed weekly with the Hamilton Rating Scale for Depression (HAMD). Allele variants were determined in each subject using a PCR-based technique. We observed a marginal association between 5-HT-2A variants and Antidepressant response while MAOA genotypes were not associated. Possible stratification factors, such as sex, diagnosis, presence of psychotic features, HAMD scores at baseline, pindolol augmentation and SSRIs plasma levels did not significantly influence the observed results. The investigated MAOA and 5-HT-2A gene variants, therefore, do not seem to play a major role in SSRI Antidepressant Activity.
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influence of tryptophan hydroxylase and serotonin transporter genes on fluvoxamine Antidepressant Activity
Molecular Psychiatry, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the A218C tryptophan hydroxylase (TPH) gene variant on the Antidepressant Activity of fluvoxamine in a sample of major and bipolar depressives, with or without psychotic features. Two hundred and seventeen inpatients were treated with fluvoxamine 300?mg and either placebo or pindolol in a double blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject by using a PCR-based technique. No significant finding was observed in the overall sample as well as in the pindolol group, while TPH*A/A was associated with a slower response to fluvoxamine treatment in subjects not taking pindolol (P = 0.001). This effect was independent from the previously reported influence of 5-HTTLPR polymorphism. If confirmed, these results may shed further light on the genetically determined component of the response to pharmacological treatments, thus helping the clinician to individualize each patient's therapy according to their genetic pattern.
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Tryptophan hydroxylase gene associated with paroxetine Antidepressant Activity.
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Cristina Cusin, Cristina Lorenzi, Enrico SmeraldiAbstract:Abstract The possible association of the A218C tryptophan hydroxylase (TPH) gene variant with the Antidepressant Activity of paroxetine was investigated in a sample of 121 inpatients affected by a major depressive episode and treated with paroxetine 20–40 mg with either placebo or pindolol in a double blind design for 4 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject using a PCR-based technique. TPH*A/A and TPH*A/C variants were associated with a poorer response to paroxetine treatment when compared to TPH*C/C ( P =0.005); this difference was not present in the pindolol augmented group. Other variables, such as sex, diagnosis, presence of psychotic features, severity of depressive symptomatology at baseline and paroxetine plasma level, were not associated with the outcome. TPH gene variants are therefore a possible modulator of paroxetine Antidepressant Activity.
Alessandro Serretti - One of the best experts on this subject based on the ideXlab platform.
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SSRIs Antidepressant Activity is influenced by Gβ3 variants
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2003Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Cristina Lorenzi, Enrico Lattuada, Adele Pirovano, Marco Catalano, Enrico SmeraldiAbstract:Abstract The aim of the present study was to test a possible effect of the G-protein β3-subunit (Gβ3) C825T gene variant on the Antidepressant Activity of selective serotonin reuptake inhibitors (SSRIs) in a sample of major and bipolar depressives, with or without psychotic features. Four hundred and ninety inpatients were treated with fluvoxamine 300 mg/day ( n =362) or paroxetine 40 mg/day ( n =128) and either placebo or pindolol in a double-blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. Gβ3 allelic variants were determined in each subject using a PCR-based technique. Subjects with Gβ3 T/T variants showed better response to treatment ( P =0.009) and this effect was independent from analyzed demographic and clinical variables. These results confirm preliminary reports and shed further light on the genetics of the response to Antidepressant treatments.
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Influence of monoamine oxidase A and serotonin receptor 2A polymorphisms in SSRI Antidepressant Activity
The international journal of neuropsychopharmacology, 2002Co-Authors: Cristina Cusin, Raffaella Zanardi, David Rossini, Roberta Lilli, Alessandro Serretti, Cristina Lorenzi, Enrico Lattuada, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the monoamine oxidase A (MAOA) and serotonin receptor 2A (5-HT-2A) gene variants on the Antidepressant Activity of fluvoxamine and paroxetine in a sample of major (n = 248) and bipolar (n = 195) depressives, with or without psychotic features. A total of 443 in-patients were treated with 300 mg fluvoxamine (n = 307) or 20-40 mg paroxetine (n = 136) for 6 wk. The severity of depressive symptoms was assessed weekly with the Hamilton Rating Scale for Depression (HAMD). Allele variants were determined in each subject using a PCR-based technique. We observed a marginal association between 5-HT-2A variants and Antidepressant response while MAOA genotypes were not associated. Possible stratification factors, such as sex, diagnosis, presence of psychotic features, HAMD scores at baseline, pindolol augmentation and SSRIs plasma levels did not significantly influence the observed results. The investigated MAOA and 5-HT-2A gene variants, therefore, do not seem to play a major role in SSRI Antidepressant Activity.
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influence of tryptophan hydroxylase and serotonin transporter genes on fluvoxamine Antidepressant Activity
Molecular Psychiatry, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the A218C tryptophan hydroxylase (TPH) gene variant on the Antidepressant Activity of fluvoxamine in a sample of major and bipolar depressives, with or without psychotic features. Two hundred and seventeen inpatients were treated with fluvoxamine 300?mg and either placebo or pindolol in a double blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject by using a PCR-based technique. No significant finding was observed in the overall sample as well as in the pindolol group, while TPH*A/A was associated with a slower response to fluvoxamine treatment in subjects not taking pindolol (P = 0.001). This effect was independent from the previously reported influence of 5-HTTLPR polymorphism. If confirmed, these results may shed further light on the genetically determined component of the response to pharmacological treatments, thus helping the clinician to individualize each patient's therapy according to their genetic pattern.
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Tryptophan hydroxylase gene associated with paroxetine Antidepressant Activity.
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Cristina Cusin, Cristina Lorenzi, Enrico SmeraldiAbstract:Abstract The possible association of the A218C tryptophan hydroxylase (TPH) gene variant with the Antidepressant Activity of paroxetine was investigated in a sample of 121 inpatients affected by a major depressive episode and treated with paroxetine 20–40 mg with either placebo or pindolol in a double blind design for 4 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject using a PCR-based technique. TPH*A/A and TPH*A/C variants were associated with a poorer response to paroxetine treatment when compared to TPH*C/C ( P =0.005); this difference was not present in the pindolol augmented group. Other variables, such as sex, diagnosis, presence of psychotic features, severity of depressive symptomatology at baseline and paroxetine plasma level, were not associated with the outcome. TPH gene variants are therefore a possible modulator of paroxetine Antidepressant Activity.
Cristina Cusin - One of the best experts on this subject based on the ideXlab platform.
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SSRIs Antidepressant Activity is influenced by Gβ3 variants
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2003Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Cristina Lorenzi, Enrico Lattuada, Adele Pirovano, Marco Catalano, Enrico SmeraldiAbstract:Abstract The aim of the present study was to test a possible effect of the G-protein β3-subunit (Gβ3) C825T gene variant on the Antidepressant Activity of selective serotonin reuptake inhibitors (SSRIs) in a sample of major and bipolar depressives, with or without psychotic features. Four hundred and ninety inpatients were treated with fluvoxamine 300 mg/day ( n =362) or paroxetine 40 mg/day ( n =128) and either placebo or pindolol in a double-blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. Gβ3 allelic variants were determined in each subject using a PCR-based technique. Subjects with Gβ3 T/T variants showed better response to treatment ( P =0.009) and this effect was independent from analyzed demographic and clinical variables. These results confirm preliminary reports and shed further light on the genetics of the response to Antidepressant treatments.
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Influence of monoamine oxidase A and serotonin receptor 2A polymorphisms in SSRI Antidepressant Activity
The international journal of neuropsychopharmacology, 2002Co-Authors: Cristina Cusin, Raffaella Zanardi, David Rossini, Roberta Lilli, Alessandro Serretti, Cristina Lorenzi, Enrico Lattuada, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the monoamine oxidase A (MAOA) and serotonin receptor 2A (5-HT-2A) gene variants on the Antidepressant Activity of fluvoxamine and paroxetine in a sample of major (n = 248) and bipolar (n = 195) depressives, with or without psychotic features. A total of 443 in-patients were treated with 300 mg fluvoxamine (n = 307) or 20-40 mg paroxetine (n = 136) for 6 wk. The severity of depressive symptoms was assessed weekly with the Hamilton Rating Scale for Depression (HAMD). Allele variants were determined in each subject using a PCR-based technique. We observed a marginal association between 5-HT-2A variants and Antidepressant response while MAOA genotypes were not associated. Possible stratification factors, such as sex, diagnosis, presence of psychotic features, HAMD scores at baseline, pindolol augmentation and SSRIs plasma levels did not significantly influence the observed results. The investigated MAOA and 5-HT-2A gene variants, therefore, do not seem to play a major role in SSRI Antidepressant Activity.
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influence of tryptophan hydroxylase and serotonin transporter genes on fluvoxamine Antidepressant Activity
Molecular Psychiatry, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the A218C tryptophan hydroxylase (TPH) gene variant on the Antidepressant Activity of fluvoxamine in a sample of major and bipolar depressives, with or without psychotic features. Two hundred and seventeen inpatients were treated with fluvoxamine 300?mg and either placebo or pindolol in a double blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject by using a PCR-based technique. No significant finding was observed in the overall sample as well as in the pindolol group, while TPH*A/A was associated with a slower response to fluvoxamine treatment in subjects not taking pindolol (P = 0.001). This effect was independent from the previously reported influence of 5-HTTLPR polymorphism. If confirmed, these results may shed further light on the genetically determined component of the response to pharmacological treatments, thus helping the clinician to individualize each patient's therapy according to their genetic pattern.
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Tryptophan hydroxylase gene associated with paroxetine Antidepressant Activity.
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Cristina Cusin, Cristina Lorenzi, Enrico SmeraldiAbstract:Abstract The possible association of the A218C tryptophan hydroxylase (TPH) gene variant with the Antidepressant Activity of paroxetine was investigated in a sample of 121 inpatients affected by a major depressive episode and treated with paroxetine 20–40 mg with either placebo or pindolol in a double blind design for 4 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject using a PCR-based technique. TPH*A/A and TPH*A/C variants were associated with a poorer response to paroxetine treatment when compared to TPH*C/C ( P =0.005); this difference was not present in the pindolol augmented group. Other variables, such as sex, diagnosis, presence of psychotic features, severity of depressive symptomatology at baseline and paroxetine plasma level, were not associated with the outcome. TPH gene variants are therefore a possible modulator of paroxetine Antidepressant Activity.
Raffaella Zanardi - One of the best experts on this subject based on the ideXlab platform.
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SSRIs Antidepressant Activity is influenced by Gβ3 variants
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2003Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Cristina Lorenzi, Enrico Lattuada, Adele Pirovano, Marco Catalano, Enrico SmeraldiAbstract:Abstract The aim of the present study was to test a possible effect of the G-protein β3-subunit (Gβ3) C825T gene variant on the Antidepressant Activity of selective serotonin reuptake inhibitors (SSRIs) in a sample of major and bipolar depressives, with or without psychotic features. Four hundred and ninety inpatients were treated with fluvoxamine 300 mg/day ( n =362) or paroxetine 40 mg/day ( n =128) and either placebo or pindolol in a double-blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. Gβ3 allelic variants were determined in each subject using a PCR-based technique. Subjects with Gβ3 T/T variants showed better response to treatment ( P =0.009) and this effect was independent from analyzed demographic and clinical variables. These results confirm preliminary reports and shed further light on the genetics of the response to Antidepressant treatments.
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Influence of monoamine oxidase A and serotonin receptor 2A polymorphisms in SSRI Antidepressant Activity
The international journal of neuropsychopharmacology, 2002Co-Authors: Cristina Cusin, Raffaella Zanardi, David Rossini, Roberta Lilli, Alessandro Serretti, Cristina Lorenzi, Enrico Lattuada, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the monoamine oxidase A (MAOA) and serotonin receptor 2A (5-HT-2A) gene variants on the Antidepressant Activity of fluvoxamine and paroxetine in a sample of major (n = 248) and bipolar (n = 195) depressives, with or without psychotic features. A total of 443 in-patients were treated with 300 mg fluvoxamine (n = 307) or 20-40 mg paroxetine (n = 136) for 6 wk. The severity of depressive symptoms was assessed weekly with the Hamilton Rating Scale for Depression (HAMD). Allele variants were determined in each subject using a PCR-based technique. We observed a marginal association between 5-HT-2A variants and Antidepressant response while MAOA genotypes were not associated. Possible stratification factors, such as sex, diagnosis, presence of psychotic features, HAMD scores at baseline, pindolol augmentation and SSRIs plasma levels did not significantly influence the observed results. The investigated MAOA and 5-HT-2A gene variants, therefore, do not seem to play a major role in SSRI Antidepressant Activity.
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influence of tryptophan hydroxylase and serotonin transporter genes on fluvoxamine Antidepressant Activity
Molecular Psychiatry, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the A218C tryptophan hydroxylase (TPH) gene variant on the Antidepressant Activity of fluvoxamine in a sample of major and bipolar depressives, with or without psychotic features. Two hundred and seventeen inpatients were treated with fluvoxamine 300?mg and either placebo or pindolol in a double blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject by using a PCR-based technique. No significant finding was observed in the overall sample as well as in the pindolol group, while TPH*A/A was associated with a slower response to fluvoxamine treatment in subjects not taking pindolol (P = 0.001). This effect was independent from the previously reported influence of 5-HTTLPR polymorphism. If confirmed, these results may shed further light on the genetically determined component of the response to pharmacological treatments, thus helping the clinician to individualize each patient's therapy according to their genetic pattern.
-
Tryptophan hydroxylase gene associated with paroxetine Antidepressant Activity.
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Cristina Cusin, Cristina Lorenzi, Enrico SmeraldiAbstract:Abstract The possible association of the A218C tryptophan hydroxylase (TPH) gene variant with the Antidepressant Activity of paroxetine was investigated in a sample of 121 inpatients affected by a major depressive episode and treated with paroxetine 20–40 mg with either placebo or pindolol in a double blind design for 4 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject using a PCR-based technique. TPH*A/A and TPH*A/C variants were associated with a poorer response to paroxetine treatment when compared to TPH*C/C ( P =0.005); this difference was not present in the pindolol augmented group. Other variables, such as sex, diagnosis, presence of psychotic features, severity of depressive symptomatology at baseline and paroxetine plasma level, were not associated with the outcome. TPH gene variants are therefore a possible modulator of paroxetine Antidepressant Activity.
David Rossini - One of the best experts on this subject based on the ideXlab platform.
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SSRIs Antidepressant Activity is influenced by Gβ3 variants
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2003Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Cristina Lorenzi, Enrico Lattuada, Adele Pirovano, Marco Catalano, Enrico SmeraldiAbstract:Abstract The aim of the present study was to test a possible effect of the G-protein β3-subunit (Gβ3) C825T gene variant on the Antidepressant Activity of selective serotonin reuptake inhibitors (SSRIs) in a sample of major and bipolar depressives, with or without psychotic features. Four hundred and ninety inpatients were treated with fluvoxamine 300 mg/day ( n =362) or paroxetine 40 mg/day ( n =128) and either placebo or pindolol in a double-blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. Gβ3 allelic variants were determined in each subject using a PCR-based technique. Subjects with Gβ3 T/T variants showed better response to treatment ( P =0.009) and this effect was independent from analyzed demographic and clinical variables. These results confirm preliminary reports and shed further light on the genetics of the response to Antidepressant treatments.
-
Influence of monoamine oxidase A and serotonin receptor 2A polymorphisms in SSRI Antidepressant Activity
The international journal of neuropsychopharmacology, 2002Co-Authors: Cristina Cusin, Raffaella Zanardi, David Rossini, Roberta Lilli, Alessandro Serretti, Cristina Lorenzi, Enrico Lattuada, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the monoamine oxidase A (MAOA) and serotonin receptor 2A (5-HT-2A) gene variants on the Antidepressant Activity of fluvoxamine and paroxetine in a sample of major (n = 248) and bipolar (n = 195) depressives, with or without psychotic features. A total of 443 in-patients were treated with 300 mg fluvoxamine (n = 307) or 20-40 mg paroxetine (n = 136) for 6 wk. The severity of depressive symptoms was assessed weekly with the Hamilton Rating Scale for Depression (HAMD). Allele variants were determined in each subject using a PCR-based technique. We observed a marginal association between 5-HT-2A variants and Antidepressant response while MAOA genotypes were not associated. Possible stratification factors, such as sex, diagnosis, presence of psychotic features, HAMD scores at baseline, pindolol augmentation and SSRIs plasma levels did not significantly influence the observed results. The investigated MAOA and 5-HT-2A gene variants, therefore, do not seem to play a major role in SSRI Antidepressant Activity.
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influence of tryptophan hydroxylase and serotonin transporter genes on fluvoxamine Antidepressant Activity
Molecular Psychiatry, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Roberta Lilli, Cristina Cusin, Enrico SmeraldiAbstract:The aim of the present study was to test a possible effect of the A218C tryptophan hydroxylase (TPH) gene variant on the Antidepressant Activity of fluvoxamine in a sample of major and bipolar depressives, with or without psychotic features. Two hundred and seventeen inpatients were treated with fluvoxamine 300?mg and either placebo or pindolol in a double blind design for 6 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject by using a PCR-based technique. No significant finding was observed in the overall sample as well as in the pindolol group, while TPH*A/A was associated with a slower response to fluvoxamine treatment in subjects not taking pindolol (P = 0.001). This effect was independent from the previously reported influence of 5-HTTLPR polymorphism. If confirmed, these results may shed further light on the genetically determined component of the response to pharmacological treatments, thus helping the clinician to individualize each patient's therapy according to their genetic pattern.
-
Tryptophan hydroxylase gene associated with paroxetine Antidepressant Activity.
European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology, 2001Co-Authors: Alessandro Serretti, Raffaella Zanardi, David Rossini, Cristina Cusin, Cristina Lorenzi, Enrico SmeraldiAbstract:Abstract The possible association of the A218C tryptophan hydroxylase (TPH) gene variant with the Antidepressant Activity of paroxetine was investigated in a sample of 121 inpatients affected by a major depressive episode and treated with paroxetine 20–40 mg with either placebo or pindolol in a double blind design for 4 weeks. The severity of depressive symptoms was weekly assessed with the Hamilton Rating Scale for Depression. TPH allelic variants were determined in each subject using a PCR-based technique. TPH*A/A and TPH*A/C variants were associated with a poorer response to paroxetine treatment when compared to TPH*C/C ( P =0.005); this difference was not present in the pindolol augmented group. Other variables, such as sex, diagnosis, presence of psychotic features, severity of depressive symptomatology at baseline and paroxetine plasma level, were not associated with the outcome. TPH gene variants are therefore a possible modulator of paroxetine Antidepressant Activity.