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Molecular Research in Antidepressant Response

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 4410

Special Issue Editors


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Guest Editor
1. Laboratory of Translational Psychiatry, Dept. of Psychiatry and Psychotherapy and Focus Program Translational Neurosciences, Johannes Gutenberg University Medical Center Mainz, 55128 Mainz, Germany
2. Leibniz Institute for Resilience Research, 55131 Mainz, Germany
Interests: depression; animal model; translational psychiatry; antidepressants; resilience; stress

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Guest Editor
1. Department of Psychiatry and Psychotherapy, University Medical Center Mainz, Untere Zahlbacher Str. 8, D-55131 Mainz, Germany
2. Laboratory of Translational Psychiatry, Dept. of Psychiatry and Psychotherapy and Focus Program Translational Neurosciences, Johannes Gutenberg University Medical Center Mainz, 55128 Mainz, Germany
Interests: depression; translational psychiatry; precision psychiatry; antidepressants; systems biology; treatment response

Special Issue Information

Dear Colleagues, 

Treating depression is not a one-size-fits-all approach. Although it would be ideal to better target available treatments to individual patients, there are no useful assessments that can predict with a reasonable high degree of certainty—a priori or early in treatment—whether a particular depressed patient will respond to a particular antidepressant.

To tackle this challenge, animal-based approaches offer the unique advantage of allowing unrestricted access to the brain and making use of the unparalleled methodological toolbox for causal manipulation. Nevertheless, studies in patients to generate hypotheses for proof-of-concept and validation of findings are an indispensable step if we are to achieve a fundamental, mechanistic understanding of the phenomenon of “response”. Moreover, the enormous importance of factors and mechanisms outside the CNS—in terms of a systems biology understanding of depression and its successful therapy—is becoming increasingly recognized. This in turn opens up entirely new perspectives on the pathophysiology of depressive disorders and their highly prevalent somatic comorbidities such as cardiovascular and metabolic diseases and offers the prospect of conceptually novel therapeutic approaches. 

With this Special Issue, we aim to advance the field by providing insights into refined animal models, improved behavioral readouts, and translationally relevant endophenotypes which can reliably inform us about the neurobiological and molecular mechanisms of antidepressant response in the animal. Moreover, we will address the phenomenon of response to antidepressant therapy from a systems biology perspective and highlight new areas of research aiming to decode the underlying molecular and systems biology (e.g., gender-related, nutritional and metabolic, inflammatory and immune) processes.

Prof. Dr. Marianne B. Müller
Dr. Jan Engelmann
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • antidepressant response
  • antidepressant signatures
  • major depressive disorder
  • animal model
  • molecular mechanism
  • systems biology
  • antidepressant biomarkers
  • depression phenotype
  • antidepressant drugs

Published Papers (2 papers)

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14 pages, 3169 KiB  
Article
Minocycline Attenuates Lipopolysaccharide-Induced Locomotor Deficit and Anxiety-like Behavior and Related Expression of the BDNF/CREB Protein in the Rat Medial Prefrontal Cortex (mPFC)
by Entesar Yaseen Abdo Qaid, Zuraidah Abdullah, Rahimah Zakaria and Idris Long
Int. J. Mol. Sci. 2022, 23(21), 13474; https://doi.org/10.3390/ijms232113474 - 3 Nov 2022
Cited by 7 | Viewed by 1571
Abstract
Neuroinflammation following lipopolysaccharide (LPS) administration induces locomotor deficits and anxiety-like behaviour. In this study, minocycline was compared to memantine, an NMDA receptor antagonist, for its effects on LPS-induced locomotor deficits and anxiety-like behaviour in rats. Adult male Sprague Dawley rats were administered either [...] Read more.
Neuroinflammation following lipopolysaccharide (LPS) administration induces locomotor deficits and anxiety-like behaviour. In this study, minocycline was compared to memantine, an NMDA receptor antagonist, for its effects on LPS-induced locomotor deficits and anxiety-like behaviour in rats. Adult male Sprague Dawley rats were administered either two different doses of minocycline (25 or 50 mg/kg/day, i.p.) or 10 mg/kg/day of memantine (i.p.) for 14 days four days prior to an LPS (5 mg/kg, i.p.) injection. Locomotor activity and anxiety-like behaviour were assessed using the open-field test (OFT). The phosphorylated tau protein level was measured using ELISA, while the expression and density of brain-derived neurotrophic factor (BDNF) and cAMP response element-binding (CREB) protein in the medial prefrontal cortex (mPFC) were measured using immunohistochemistry and Western blot, respectively. Minocycline treatment reduced locomotor deficits and anxiety-like behaviour associated with reduced phosphorylated tau protein levels, but it upregulated BDNF/CREB protein expressions in the mPFC in a comparable manner to memantine, with a higher dose of minocycline having better benefits. Minocycline treatment attenuated LPS-induced locomotor deficits and anxiety-like behaviour in rats and decreased phosphorylated tau protein levels, but it increased the expressions of the BDNF/CREB proteins in the mPFC. Full article
(This article belongs to the Special Issue Molecular Research in Antidepressant Response)
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16 pages, 1499 KiB  
Article
Antidepressant Effect of Intermittent Long-Term Systemic Administration of Irisin in Mice
by Patrizia Pignataro, Manuela Dicarlo, Roberta Zerlotin, Giuseppina Storlino, Angela Oranger, Lorenzo Sanesi, Roberto Lovero, Cinzia Buccoliero, Giorgio Mori, Graziana Colaianni, Silvia Colucci and Maria Grano
Int. J. Mol. Sci. 2022, 23(14), 7596; https://doi.org/10.3390/ijms23147596 - 8 Jul 2022
Cited by 13 | Viewed by 2370
Abstract
Depression is a psychiatric disorder increasingly diffused worldwide. Evidence suggests that irisin, a myokine secreted by contracting muscle, mediates beneficial effects on several targets, including the brain. Here, the potential antidepressant properties of long-term intermittent systemic irisin administration (100 µg/kg/weekly for 1 month) [...] Read more.
Depression is a psychiatric disorder increasingly diffused worldwide. Evidence suggests that irisin, a myokine secreted by contracting muscle, mediates beneficial effects on several targets, including the brain. Here, the potential antidepressant properties of long-term intermittent systemic irisin administration (100 µg/kg/weekly for 1 month) were evaluated in mice by the Tail Suspension Test (TST), Forced Swim Test (FST), and Open Field Test (OFT). Furthermore, to deepen the molecular pathways underlying irisin treatment, the expression of irisin precursor, neurotrophic/growth factors, and cytokines was analyzed. Irisin treatment significantly decreased the immobility time in the TST and FST, suggesting an antidepressant effect. Additionally, irisin seemed to display an anxiolytic-like effect increasing the time spent in the OFT arena center. These findings were probably due to the modulation of endogenous brain factors as the gene expression of some neurotrophins, such as brain-derived neurotrophic factor (BDNF) and insulin-like growth factor (IGF-1), was upregulated only in irisin-treated mouse brain. Moreover, irisin modulated the expression of some cytokines (IL-1β, IL-4, IL-6, and IL-10). To the best of our knowledge, this is the first study demonstrating that the irisin antidepressant effect may be observed even with a systemic administration in mice. This could pave the way toward intriguing preclinical research in humans. Full article
(This article belongs to the Special Issue Molecular Research in Antidepressant Response)
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