Is treatment-resistance in unipolar melancholic depression characterized by decreased serotonin2A receptors in the dorsal prefrontal – Anterior cingulate cortex?

Baeken, Chris; Raedt, Rudi De; Bossuyt, Axel

doi:10.1016/j.neuropharm.2011.07.043

Cited by 22 publications

(15 citation statements)

References 43 publications

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“…Altered serotonergic function, such as decreased post-synaptic 5-HT-2A receptors in the dorsal regions of the prefrontal and the anterior cingulate cortex, were observed in antidepressant-free TRD patients (Baeken et al 2012). However, the results of the present study show no differences between patients with and without TRD in the frequency of components of MetS, BMI and both atherogenic index 1 and 2.…”

Section: Discussioncontrasting

confidence: 72%

The lack of association between components of metabolic syndrome and treatment resistance in depression

et al. 2013

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(2013) The lack of association between components of metabolic syndrome and treatment resistance in depression. npivac@irb.hr Psychopharmacology, 230 (1). Conflicts of Interest:Authors declare no conflict of interest. All authors state that they have full control of all primary data and that they agree to allow the journal to review this data. Acknowledgments:This study was supported by the Croatian Ministry of Science, Education and Sport, grants numbers 098-0982522-2455; 098-0982522-2457; 109-1083509-3513; 108-1083509-3511.

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Section: Discussioncontrasting

confidence: 72%

The lack of association between components of metabolic syndrome and treatment resistance in depression

et al. 2013

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“…Among individuals with depression, suicidality has been shown to be associated with greater feelings of desperation (Garlow et al, 2008) and hopelessness (Nyer et al, 2013). Prior studies have also shown that there are structural dACC differences in MDD patients who are and are not at risk for suicide (Wagner et al, 2011), and that dACC functioning is associated with treatment-resistant depression (Baeken et al, 2012). Taken together, it is possible that specific subgroups of depressed individuals, namely those with suicidality, evidence abnormal dACC reactivity and experience the greatest affective conflict during reward anticipation due to the fact that the context is starkly incongruent with their hopeless and/or pessimistic mood.…”

Section: Discussionmentioning

confidence: 99%

Neural response to reward anticipation in those with depression with and without panic disorder

Gorka¹,

Huggins²,

Fitzgerald³

et al. 2014

Journal of Affective Disorders

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Background One of the hallmark features of major depressive disorder (MDD) is reduced reward anticipation. There have been mixed findings in the literature as to whether reward anticipation deficits in MDD are related to diminished mesolimbic activation and/or enhanced dorsal anterior cingulate activation (dACC). One of the reasons for these mixed findings is that these studies have typically not addressed the role of comorbid anxiety, a class of disorders which frequently co-occur with depression and have a common neurobiology. Methods The aim of the current study was to examine group differences in neural responses to reward anticipation in 40 adults with either: 1) current MDD with no lifetime diagnosis of an anxiety disorder (MDD-only), 2) current MDD with comorbid panic disorder (MDD-PD), or 3) no lifetime diagnosis of psychopathology. All participants completed a passive slot machine task during a functional magnetic resonance imaging (fMRI) scan. Results Analyses indicated that there were no group differences in activation of mesolimbic reward regions; however, the MDD-only group exhibited greater dACC activation during the anticipation of rewards compared with the healthy controls and the comorbid MDD-PD group (who did not differ from each other). Limitations The sample size was small which limits generalizability. Conclusions These findings provide preliminary support for the role of hyperactive dACC functioning in reduced reward anticipation in MDD. They also indicate that comorbid anxiety may alter the association between MDD and neural responding to reward anticipation.

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“…In a study using the radioligand 123 I-5-I-R91150 with single photon emission computed tomography in TRD patients, it could be demonstrated that the postsynaptic serotonin 5-HT 2A receptors in dorsal regions of the prefrontal and the ACC are down-regulated compared to never depressed controls, whereas 5-HT 2A receptor binding did not differ from controls in first-episode depressed patients (Baeken, De Raedt & Bossuyt, 2012). Based on these findings, the effect of 10 daily weekday HF-rTMS sessions applied to the left DLPFC on postsynaptic 5-HT 2A receptor binding indices was examined in a group of antidepressant-free, pharmaco-resistant depressed (TRD) patients .…”

Section: Molecular Approach To Working Mechanisms Of Neurostimulationmentioning

confidence: 99%

Neurostimulation as an intervention for treatment resistant depression: From research on mechanisms towards targeted neurocognitive strategies

Raedt

Vanderhasselt

Baeken

2015

Clinical Psychology Review

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105

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Despite the fact that several interventions for major depression have proven efficacy, a substantial number of patients are or become treatment resistant to various forms of pharmacotherapy and psychotherapy. Biological interventions that directly target brain activity such as electroconvulsive therapy are used to treat these patients, but some of these interventions are unlikely to be easily accepted because of their more invasive nature or sideeffects. The efficacy of non-invasive neurostimulation with a favorable side effect profile, such as repetitive Transcranial Magnetic Stimulation, could not be sufficiently demonstrated for treatment resistant depressed patients (TRD). We argue that research on the working mechanisms of these neurostimulation techniques is necessary to develop more efficient treatment protocols. After an overview of current neurostimulation approaches to treatment resistance and the introduction of a neurobiological and a cognitive framework of depression, we provide an integrative review of research on both the neurobiological and cognitive working mechanisms of neurostimulation in TRD, with a specific emphasis on the work of our lab. Thereafter, we describe our own studies and studies from other labs on new neurocognitive interventions. Finally we discuss how all this knowledge can be used to further develop new strategies to deal with treatment resistance, in combining neurostimulation and cognitive interventions.

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Is treatment-resistance in unipolar melancholic depression characterized by decreased serotonin2A receptors in the dorsal prefrontal – Anterior cingulate cortex?

Cited by 22 publications

References 43 publications

The lack of association between components of metabolic syndrome and treatment resistance in depression

The lack of association between components of metabolic syndrome and treatment resistance in depression

Neural response to reward anticipation in those with depression with and without panic disorder

Neurostimulation as an intervention for treatment resistant depression: From research on mechanisms towards targeted neurocognitive strategies

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