Quetiapine augmentation in depressed patients with partial response to antidepressants

Olver, James S; Ignatiadis, S; Maruff, Paul; Burrows, Graham D.; Norman, Trevor R.

doi:10.1002/hup.970

Cited by 23 publications

(13 citation statements)

References 33 publications

(46 reference statements)

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“…However, in schizophrenia, data strongly suggest that atypical ones in particular either have no effect or improve executive functioning (Meyer-Lindberg et al 1997 ;Burke et al 1998 ;Cuesta et al 2001 ;Velligan et al 2002 ;McGurk et al 2004 ;Mishara & Goldberg, 2004 ;Tyson et al 2004 ;Woodwart et al 2005 ;O'Grada & Dinan, 2007). In depression, data on the cognitive effects of antipsychotics are sparse but in the same direction (Olver et al 2008 ;Frasch et al 2009). …”

Section: Comparison Of Clinical Profilesmentioning

confidence: 89%

Contrasting patterns of deficits in visuospatial memory and executive function in patients with major depression with and without ECT referral

et al. 2010

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Section: Comparison Of Clinical Profilesmentioning

confidence: 89%

Contrasting patterns of deficits in visuospatial memory and executive function in patients with major depression with and without ECT referral

et al. 2010

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“…In treatment-resistant depression, co-administration of modest doses of atypical APDs to SSRIs or SNRIs has been shown to augment the antidepressant effect with a rapid onset of action, i.e. appearing within days compared to weeks with antidepressant drugs alone (Debattista and Hawkins, 2009;Mahmoud et al, 2007;Nelson and Papakostas, 2009;Nemeroff, 2005;Olver et al, 2008;Tohen et al, 2010), although the mechanisms involved are not fully understood.…”

Section: Apds In the Pharmacotherapy Of Major Depressive Disordermentioning

confidence: 99%

Involvement of 5‐HT_2A receptor and α₂‐adrenoceptor blockade in the asenapine‐induced elevation of prefrontal cortical monoamine outflow

Frånberg¹,

Marcus²,

Svensson³

2012

Synapse

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The psychotropic drug asenapine is approved for the treatment of schizophrenia and manic or mixed episodes associated with bipolar I disorder. Asenapine exhibits higher affinity for several 5-HT receptors and α(2)-adrenoceptors than for D(2) receptors. Noteworthy, blockage of both the 5-HT(2A) and α(2)-adrenergic receptors has been shown to enhance prefrontal dopamine release induced by D(2) receptor antagonists. Previous results show that asenapine, both systemically and locally, increases dopamine, noradrenaline, and serotonin release in the medial prefrontal cortex (mPFC), and that the increased dopamine release largely depends on an intracortical action. Using reverse microdialysis in freely moving rats, we here assessed the potency of low concentrations of asenapine to cause a pharmacologically significant blockage in vivo of 5-HT(2A) receptors and α(2)-adrenoceptors within the mPFC, and thus its ability to affect cortical monoamine release by these receptors. Intracortical administration of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI), a 5-HT(2A/2C) receptor agonist, increased cortical monoamine release, effects that were antagonized both by asenapine and the selective 5-HT(2A) antagonist M100907. Application of clonidine, an α(2)-adrenoceptor agonist, significantly reduced monoamine release in the mPFC. The selective α(2)-adrenoceptor antagonist idazoxan blocked, whereas asenapine partially blocked clonidine-induced cortical dopamine and noradrenaline decrease. The effects of asenapine and idazoxan on clonidine-induced serotonin decrease were less pronounced. Our results propose that low concentrations of asenapine in the mPFC exhibit a pharmacologically significant 5-HT(2A) and α(2) receptor antagonistic activity, which may contribute to enhance prefrontal monoamine release in vivo and, secondarily, its clinical effects in schizophrenia and bipolar disorder.

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“…However, although the combination of quetiapine in addition to SSRIs has been proven to be beneficial in neuropsychiatric disorders including depression (Chertkow et al, 2009;Devarajan et al, 2006), the impact of this augmentation strategy on cognitive functions has not been systematically addressed in either clinical trials or preclinical models. Nevertheless, some reports suggest that clinical benefits of quetiapine augmentation of SSRI antidepressant therapy may include possible improvements in cognition (Olver et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Quetiapine ameliorates stress-induced cognitive inflexibility in rats

Nikiforuk¹

2013

Neuropharmacology

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Quetiapine augmentation in depressed patients with partial response to antidepressants

Abstract: This suggests clinical benefits of quetiapine augmentation of SSRI/SNRI antidepressants with no worsening, and possible improvements in cognition.

Cited by 23 publications

References 33 publications

Contrasting patterns of deficits in visuospatial memory and executive function in patients with major depression with and without ECT referral

Contrasting patterns of deficits in visuospatial memory and executive function in patients with major depression with and without ECT referral

Involvement of 5‐HT_2A receptor and α₂‐adrenoceptor blockade in the asenapine‐induced elevation of prefrontal cortical monoamine outflow

Quetiapine ameliorates stress-induced cognitive inflexibility in rats

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Quetiapine augmentation in depressed patients with partial response to antidepressants

Abstract: This suggests clinical benefits of quetiapine augmentation of SSRI/SNRI antidepressants with no worsening, and possible improvements in cognition.

Cited by 23 publications

References 33 publications

Contrasting patterns of deficits in visuospatial memory and executive function in patients with major depression with and without ECT referral

Contrasting patterns of deficits in visuospatial memory and executive function in patients with major depression with and without ECT referral

Involvement of 5‐HT2A receptor and α2‐adrenoceptor blockade in the asenapine‐induced elevation of prefrontal cortical monoamine outflow

Quetiapine ameliorates stress-induced cognitive inflexibility in rats

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Involvement of 5‐HT_2A receptor and α₂‐adrenoceptor blockade in the asenapine‐induced elevation of prefrontal cortical monoamine outflow