A prospective, longitudinal study of platelet serotonin and plasma brain-derived neurotrophic factor concentrations in major depression: effects of vortioxetine treatment

Šagud, Marina; Perković, Matea Nikolac; Vuksan-Ćusa, Bjanka; Maravic, Anja; Štrac, Dubravka Švob; Peleš, Alma Mihaljević; Živković, Maja; Kušević, Zorana; Pivac, Nela

doi:10.1007/s00213-016-4364-0

Cited by 35 publications

(31 citation statements)

References 52 publications

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“…139 In patients with major depressive disorder, lower basal plasma BDNF levels have been described consistently, and chronic antidepressant treatment was associated with increased plasma BDNF levels in accordance with clinical improvement. [140][141][142] A post-mortem analysis also found an AD-mediated increase of BDNF levels in multiple brain regions. 143 In non-responders, BDNF levels remained significantly lower.…”

Section: Therapeutic Relevance Of Bdnf Signallingmentioning

confidence: 86%

Changes in neuroplasticity following early-life social adversities: the possible role of brain-derived neurotrophic factor

2018

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Social adversities experienced in childhood can have a profound impact on the developing brain, leading to the emergence of psychopathologies in adulthood. Despite the burden this places on both the individual and society, the neurobiological aspects mediating this transition remain unclear. Recent advances in preclinical and clinical research have begun examining neuroplasticity-the nervous system's ability to form adaptive changes in response to new experience-in the context of early-life vulnerability to social adversities and plasticity-related alterations following such traumatic events. A key mediator of plasticity-related molecular processes is the brain-derived neurotrophic factor (BDNF), which has also been implicated in various psychiatric disorders related to childhood social adversities. Preclinical and clinical data suggest early-life social adversities (ELSA) might be associated with accelerated maturation of social network circuitry, a possible ontogenic adaptation to the adverse environment. Neural plasticity decreases by adulthood, lessening the efficacy of treatment in ELSA-related psychiatric disorders. However, literature data suggest that by increasing BDNF/TrkB signalling through antidepressant treatment a juvenile-like plasticity state can be induced, which allows for reorganization of the social circuitry when guided by psychotherapy and surrounded by a safe and positive environment.

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Section: Therapeutic Relevance Of Bdnf Signallingmentioning

confidence: 86%

Changes in neuroplasticity following early-life social adversities: the possible role of brain-derived neurotrophic factor

2018

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“…First, the CUMS procedure in our study may not be strong enough to change the expression of the t5-HT 1A receptor in the hippocampus of tested mice. Second, the 5-HT level decrease in the hippocampus may be a consequence of other receptors' interplay or signaling pathways like the brain derived neurotrophic factor (BDNF), since several studies suggested that 5-HT can stimulate the BDNF gene or protein expression in depressive patients (14) and rodents (15). Further studies are therefore necessary to elucidate this issue.…”

Section: Lmmcs Did Not Change the 5-ht 1a Protein Expression In The Hmentioning

confidence: 99%

Low molecular mass chondroitin sulfate suppresses chronic unpredictable mild stress-induced depression-like behavior in mice

Tian

Zhang

et al. 2018

Acta Pharmaceutica

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The present study is aimed at testing the antidepressant--like effects and probable mechanisms of action of low molecular mass chondroitin sulfate (LMMCS) on depression induced by chronic unpredictable mild stress (CUMS) in mice. Four weeks of CUMS exposure resulted in depressive-like behavior, expressed by a significant decrease in the locomotor activity and sucrose consumption and increased immobility time in the forced swim test. Further, there was a significant reduction of 5-HT level in the hippocampus region of depressed mice. Treatment of mice for four weeks with LMMCS ameliorated significantly both the behavioral and biochemical changes induced by CUMS. These novel results suggest that LMMCS produces an antidepressant-like effect in mice subjected to CUMS, which might be related, at least in part, to the increase of 5-HT concentration in the hippocampus.

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“…This compound blocks the SERT as well multiple 5-HT receptors (Sanchez et al, 2015; Sagud et al, 2016). This effect is in line with studies reporting that the combination of antidepressants with atypical antipsychotic drugs (olanzapine, risperidone, quetiapine, aripiprazole, paliperidone, ziprazidone, and amisulpride), can boost the effectiveness of depression treatment (Berman et al, 2007; Thase et al, 2007; Bauer et al, 2009; Han et al, 2013).…”

Section: From the Drugs To Monoaminesmentioning

confidence: 99%

Monoaminergic and Histaminergic Strategies and Treatments in Brain Diseases

et al. 2016

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The monoaminergic systems are the target of several drugs for the treatment of mood, motor and cognitive disorders as well as neurological conditions. In most cases, advances have occurred through serendipity, except for Parkinson's disease where the pathophysiology led almost immediately to the introduction of dopamine restoring agents. Extensive neuropharmacological studies first showed that the primary target of antipsychotics, antidepressants, and anxiolytic drugs were specific components of the monoaminergic systems. Later, some dramatic side effects associated with older medicines were shown to disappear with new chemical compounds targeting the origin of the therapeutic benefit more specifically. The increased knowledge regarding the function and interaction of the monoaminergic systems in the brain resulting from in vivo neurochemical and neurophysiological studies indicated new monoaminergic targets that could achieve the efficacy of the older medicines with fewer side-effects. Yet, this accumulated knowledge regarding monoamines did not produce valuable strategies for diseases where no monoaminergic drug has been shown to be effective. Here, we emphasize the new therapeutic and monoaminergic-based strategies for the treatment of psychiatric diseases. We will consider three main groups of diseases, based on the evidence of monoamines involvement (schizophrenia, depression, obesity), the identification of monoamines in the diseases processes (Parkinson's disease, addiction) and the prospect of the involvement of monoaminergic mechanisms (epilepsy, Alzheimer's disease, stroke). In most cases, the clinically available monoaminergic drugs induce widespread modifications of amine tone or excitability through neurobiological networks and exemplify the overlap between therapeutic approaches to psychiatric and neurological conditions. More recent developments that have resulted in improved drug specificity and responses will be discussed in this review.

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A prospective, longitudinal study of platelet serotonin and plasma brain-derived neurotrophic factor concentrations in major depression: effects of vortioxetine treatment

Abstract: Conflict of interestThe authors declare no conflicts of interest in relation to the current study, and in general. Abstract Background

Cited by 35 publications

References 52 publications

Changes in neuroplasticity following early-life social adversities: the possible role of brain-derived neurotrophic factor

Changes in neuroplasticity following early-life social adversities: the possible role of brain-derived neurotrophic factor

Low molecular mass chondroitin sulfate suppresses chronic unpredictable mild stress-induced depression-like behavior in mice

Monoaminergic and Histaminergic Strategies and Treatments in Brain Diseases

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