Single ketamine infusion in bipolar depression resistant to antidepressants: are neurotrophins involved?

Rybakowski, Janusz; Permoda-Osip, Agnieszka; Skibińska, Maria; Adamski, R.; Bartkowska-Śniatkowska, Alicja

doi:10.1002/hup.2271

Cited by 84 publications

(57 citation statements)

References 17 publications

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“…Thirtyfive studies, comprising a total of 2238 bipolar disorder patients and 1560 healthy control subjects, were eligible for review and included in the meta-analysis with a minimum of one pair-wise comparison each. [11][12][13][19][20][21]26, Exclusion of full 63 text articles and reports were based on (a) data on BDNF levels were unavailable, [66][67][68] (b) patients not suffering from bipolar disorder, [69][70][71][72][73][74][75][76][77][78][79][80][81][82][83][84] (c) the study not evaluating peripheral BDNF levels, (d) the study being a review or a comment, [107][108][109][110][111][112][113][114][115][116][117][118][119] (e) the study not comparing states or comparing bipolar patients with healthy control subjects [120][121][122] and/or (f) the study investigated treatment of experimental nature 123,124 and (g) the study presenting duplicate data presented in an included article. …”

Section: Study Selectionmentioning

confidence: 99%

Peripheral blood brain-derived neurotrophic factor in bipolar disorder: a comprehensive systematic review and meta-analysis

2015

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Peripheral blood brain-derived neurotrophic factor (BDNF) has been proposed as a potential biomarker related to disease activity and neuroprogression in bipolar disorder, speculated to mirror alterations in brain expression of BDNF. The research area is rapidly evolving; however, recent investigations have yielded conflicting results with substantial variation in outcomes, highlighting the need to critically assess the state of current evidence. The aims of the study were to investigate differences in peripheral blood BDNF concentrations between bipolar disorder patients and healthy control subjects and between affective states in bipolar disorder patients, including assessment of the effect of treatment of acute episodes on BDNF levels. A systematic review of English language studies without considering publication status was conducted in PubMed (January 1950-November 2014), Embase (1974-November 2014) and PsycINFO (1806-November 2014), and 35 studies comprising a total of 3798 participants were included in the meta-analysis. The results indicated that crude peripheral blood BDNF levels may be lower in bipolar disorder patients overall (Hedges' g=-0.28, 95% CI: -0.51 to -0.04, P=0.02) and in serum of manic (g=-0.77, 95% CI: -1.36 to -0.18, P=0.01) and depressed (g=-0.87, 95% CI: -1.42 to -0.32, P=0.002) bipolar disorder patients compared with healthy control subjects. No differences in peripheral BDNF levels were observed between affective states overall. Longer illness duration was associated with higher BDNF levels in bipolar disorder patients. Relatively low study quality, substantial unexplained between-study heterogeneity, potential bias in individual studies and indications of publication bias, was observed and studies were overall underpowered. It could thus not be excluded that identified differences between groups were due to factors not related to bipolar disorder. In conclusion, limitations in the evidence base prompt tempered conclusions regarding the role of peripheral BDNF as a biomarker in bipolar disorder and substantially improving the quality of further research is warranted.

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Section: Study Selectionmentioning

confidence: 99%

Peripheral blood brain-derived neurotrophic factor in bipolar disorder: a comprehensive systematic review and meta-analysis

2015

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“…Activated astrocytes also secrete several neurotrophic factors, e.g., glial-derived neurotrophic factor (GDNF). In addition to its neuroprotective role, serum GDNF levels are reduced in major depression [including adolescent (Pallavi et al 2013) and late-life depression (Diniz et al 2012)] and has been improved by antidepressant treatment in both preclinical (Liu et al 2012a) and clinical studies (Zhang et al 2008; Zhang et al 2009) [although a recent report noted no change in peripheral GDNF levels by ketamine in bipolar depression (Rybakowski et al 2013)].…”

Section: Glutamate and Its Receptors In The Pathophysiology And Treatmentioning

confidence: 99%

Glutamate and its receptors in the pathophysiology and treatment of major depressive disorder

et al. 2013

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Monoaminergic neurotransmitter (serotonin, norepinephrine and dopamine) mechanisms of disease dominated the research landscape in the pathophysiology and treatment of major depressive disorder (MDD) for more than 50 years and still dominate available treatment options. However, the sum of all brain neurons that use monoamines as their primary neurotransmitter is <20 %. In addition, most patients treated with monoaminergic antidepressants are left with significant residual symptoms and psychosocial disability not to mention side effects, e.g., sexual dysfunction. In the past several decades, there has been greater focus on the major excitatory neurotransmitter in the human brain, glutamate, in the pathophysiology and treatment of MDD. Although several preclinical and human magnetic resonance spectroscopy studies had already implicated glutamatergic abnormalities in the human brain, it was rocketed by the discovery that the N-methyl-D-aspartate receptor antagonist ketamine has rapid and potent antidepressant effects in even the most treatment-resistant MDD patients, including those who failed to respond to electroconvulsive therapy and who have active suicidal ideation. In this review, we will first provide a brief introduction to glutamate and its receptors in the mammalian brain. We will then review the clinical evidence for glutamatergic dysfunction in MDD, the discovery and progress-to-date with ketamine as a rapidly acting antidepressant, and other glutamate receptor modulators (including proprietary medications) for treatment-resistant depression. We will finally conclude by offering potential future directions necessary to realize the enormous therapeutic promise of glutamatergic antidepressants.

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“…In the clinic, except for one initial contradictory report [60], a series of recent investigations consistently reported elevated serum BDNF in samples of frequent ketamine users [61], treatmentresistant major depression patients responding to ketamine treatment [62,63] and bipolar patients responding to ketamine [64]. Likewise, phMRI investigations on subanaesthetic doses of ketamine in healthy volunteers showed activation in many regions of the brain including cingulate cortex (midline, supra, anterior and posterior aspects), prefrontal cortex (medial, ventrolateral and dorsolateral), thalamus, insula and anterior temporal lobe, and more interestingly, a decrease in blood oxygen level dependent (BOLD) signal in the subgenual cingulate cortex [14,65,66].…”

Section: Antidepressant Mechanisms Of Ketaminementioning

confidence: 98%

Ketamine and suicidal ideation in depression: Jumping the gun?

Rajkumar

Fam

Yeo

et al. 2015

Pharmacological Research

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Single ketamine infusion in bipolar depression resistant to antidepressants: are neurotrophins involved?

Abstract: The results confirm an antidepressant effect of ketamine infusion as an add-on to mood-stabilizing drugs in bipolar depression resistant to antidepressant treatment. They may also suggest a possible involvement of BDNF in this effect.

Cited by 84 publications

References 17 publications

Peripheral blood brain-derived neurotrophic factor in bipolar disorder: a comprehensive systematic review and meta-analysis

Peripheral blood brain-derived neurotrophic factor in bipolar disorder: a comprehensive systematic review and meta-analysis

Glutamate and its receptors in the pathophysiology and treatment of major depressive disorder

Ketamine and suicidal ideation in depression: Jumping the gun?

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