Differentiation of two genetically specific types of depression by the response to antidepressant drugs.

Pare, C. M. B.; Mack, Jennifer W.

doi:10.1136/jmg.8.3.306

Cited by 109 publications

(37 citation statements)

References 5 publications

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“…With MAOIs falling into disuse, it seems unlikely that more pharmacologic trials will be performed to further address these issues. Thirty years ago, using antidepressant response rates in probands and family members, Pare and Mack 48 suggested that certain patients may have a distinct genetic makeup that predisposes them to respond to particular antidepressants. Since then, little progress has been made in our ability to profile specific antidepressant responders.…”

Section: Commentmentioning

confidence: 99%

Partial Validation of the Atypical Features Subtype of Major Depressive Disorder

Posternak¹,

Zimmerman²

2002

Arch Gen Psychiatry

102

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Background: Symptoms of the atypical features subtype of major depressive disorder include mood reactivity, hypersomnia, hyperphagia, leaden paralysis, and rejection sensitivity. This subtype was introduced into the mood disorders section of the DSM-IV following a series of antidepressant trials showing that such patients responded preferentially to monoamine oxidase inhibitors. Studies aimed at validating the atypical features subtype have yielded inconsistent results. Our study sought to reevaluate the validity of atypical depression by examining the demographic and clinical features of a large cohort of depressed patients who met DSM-IV criteria for atypical features.

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Section: Commentmentioning

confidence: 99%

Partial Validation of the Atypical Features Subtype of Major Depressive Disorder

Posternak¹,

Zimmerman²

2002

Arch Gen Psychiatry

102

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“…[1][2][3][4][5][6][7] Selective serotonin reuptake inhibitors (SSRIs) exert their activity through a blockade of the neuronal serotonin transporter. The gene encoding for this protein has been shown to have a functional polymorphism in the upstream regulatory region (5-HTTLPR) 8,9 and recent studies have reported an association between this polymorphism and the antidepressant response to certain SSRIs, such as fluvoxamine 10,11 and paroxetine.…”

mentioning

confidence: 99%

Influence of tryptophan hydroxylase and serotonin transporter genes on fluvoxamine antidepressant activity

et al. 2001

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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 Antidepressant drugs efficacy for major depression treatment is partly under genetic control.

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“…The difference between patients who respond to mono-amine-oxi dase inhibitors (MAOis) and those who respond to the imipramine group of antidepressant s may, indeed, be based on genetic factors (Angst 1961;Pare et al 1962;Pare and Mack 1971) as first degree relatives who become depressed, will also respond to these dxugs in a similar way.…”

Section: A High Incidence Of Suicide In the Relatives Of Bipolar Patimentioning

confidence: 99%

Depression in Patients With Epilepsy

Robertson¹

1984

Clinical Neuropharmacology

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Differentiation of two genetically specific types of depression by the response to antidepressant drugs.

Cited by 109 publications

References 5 publications

Partial Validation of the Atypical Features Subtype of Major Depressive Disorder

Partial Validation of the Atypical Features Subtype of Major Depressive Disorder

Influence of tryptophan hydroxylase and serotonin transporter genes on fluvoxamine antidepressant activity

Depression in Patients With Epilepsy

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