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Molecular Insights into Neurotrophins and Neuropsychiatric Disorders
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Molecular Insights into Neurotrophins and Neuropsychiatric Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 11762

Special Issue Editors

Dr. Marco Fiore

E-Mail Website
Guest Editor
Institute of Biochemistry and Cell Biology (IBBC), National Research Council (CNR), Department of Sense Organs, University Sapienza of Rome, Viale del Policlinico, Rome, Italy
Interests: neurobiology; endocrinology; neurotrophins; oxidative stress; cancer; toxicology; addiction; antioxidants; polyphenols; alcohol use disorders
Special Issues, Collections and Topics in MDPI journals
Dr. Giampiero Ferraguti

E-Mail Website
Guest Editor
Department of Experimental Medicine, Sapienza University of Rome, 00185 Rome, Italy
Interests: addiction biology; toxicology; clinical biochemistry; genetics and molecular biology; neurobiology of alcohol use disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the intricate landscape of neuroscience, the interplay between molecular mechanisms and neuropsychiatric disorders has long intrigued researchers. Among the key players in this arena are neurotrophins, a family of proteins crucial for the development, function, and survival of neurons in the nervous system. Over recent decades, mounting evidence has underscored the pivotal role of neurotrophins in various aspects of brain function, including synaptic plasticity, neuronal survival, and neurogenesis.

Understanding the molecular underpinnings of neurotrophins has not only shed light on fundamental processes in neurobiology but has also unveiled promising avenues for deciphering the complexities of neuropsychiatric disorders. From depression and anxiety to schizophrenia and neurodegenerative diseases, the dysregulation of neurotrophin signaling pathways has been implicated in the pathogenesis and progression of myriad mental health conditions.

This synthesis of molecular insights into neurotrophins and neuropsychiatric disorders represents a frontier in neuroscience research, offering both theoretical frameworks and practical implications for the diagnosis, treatment, and prevention of these debilitating conditions. By unraveling the intricate dance between neurotrophins and the brain’s circuitry, researchers are poised to unlock novel therapeutic targets and interventions that have the potential to alleviate the burden of neuropsychiatric disorders on individuals and society as a whole.

This Special Issue focuses on the current understanding of and future research directions regarding Molecular Insights into Neurotrophins and Neuropsychiatric Disorders. We warmly welcome original research and review articles relating to this crucial topic.

Dr. Marco Fiore
Dr. Giampiero Ferraguti
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • growth factors
  • neurotrophins
  • NGF
  • BDNF
  • neurodegeneration
  • brain diseases
  • NT-3
  • NT- 4
  • neurotrophin receptors

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Published Papers (4 papers)

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Research

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22 pages, 1810 KiB  
Article
Progesterone Promotes Anti-Anxiety/Depressant-like Behavior and Trophic Actions of BDNF in the Hippocampus of Female Nuclear Progesterone Receptor, but Not 5α-Reductase, Knockout Mice
by Cheryl A. Frye, Daina M. Cleveland, Anjali Sadarangani and Jennifer K. Torgersen
Int. J. Mol. Sci. 2025, 26(3), 1173; https://doi.org/10.3390/ijms26031173 - 29 Jan 2025
Viewed by 833
Abstract
Progestogens’ anti-anxiety and anti-depressive effects and mechanisms are not well-understood. Progestogens are hypothesized to have anti-anxiety and anti-depressive effects on behavior, independent of actions at nuclear progestin receptors (NPRs) and dependent on allopregnanolone (5α-pregnan-3α-ol-20-one; 3α,5α-THP), a 5α-reduced, neuroactive metabolite of progesterone (P4 [...] Read more.
Progestogens’ anti-anxiety and anti-depressive effects and mechanisms are not well-understood. Progestogens are hypothesized to have anti-anxiety and anti-depressive effects on behavior, independent of actions at nuclear progestin receptors (NPRs) and dependent on allopregnanolone (5α-pregnan-3α-ol-20-one; 3α,5α-THP), a 5α-reduced, neuroactive metabolite of progesterone (P4). Adult c57 mice in behavioral estrus (proestrus; pro) showed more anti-anxiety-like and anti-depressant-like behavior and higher levels of estradiol (E2), P4, and allopregnanolone in the hippocampus/amygdala complex. Proestrus c57 > 5α-reductase knockout (5αRKO) mice made more central entries in an open field than diestrus c57 and 5αRKO mice that were not different. Ovariectomized (OVX) c57 mice administered 1, 2, or 4 mg/kg P4 SC showed dosage-dependent increases in central entries in an open field (more anti-anxiety-like behavior); 5αRKO mice had maximal increases at 1–2 mg/kg P4. OVX c57 and 5αRKO mice showed maximum increases in central entries with SC 3α,5α-THP (4 mg/kg), and c57s showed a similar maximal response to P4 (4 mg/kg), but 5αRKOs response was half at that dosage. P4 (4 mg/kg SC to OVX c57 or progestin receptor knockout (PRKO) mice decreased immobility (depression-like behavior) in the forced swim task. Effects of E2 and veh were similar in both groups. Levels of 3α,5α-THP in the hippocampus/amygdala were consistent with effects on central entries in the open field. Levels of brain-derived neurotrophic factor (BDNF) in the hippocampus/amygdala were greater among E2-primed (0.09 mg/kg, SC) vs vehicle-administered mice. In sum, adult female mice can be responsive to P4 for anti-anxiety/anti-depressant-like behavior; such effects may be independent of NPRs but require 5α-reduction and E2’s priming actions at BDNF in the hippocampus/amygdala complex. Full article
(This article belongs to the Special Issue Molecular Insights into Neurotrophins and Neuropsychiatric Disorders)
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Review

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19 pages, 1213 KiB  
Review
Variations in BDNF and Their Role in the Neurotrophic Antidepressant Mechanisms of Ketamine and Esketamine: A Review
by Simone Pardossi, Andrea Fagiolini and Alessandro Cuomo
Int. J. Mol. Sci. 2024, 25(23), 13098; https://doi.org/10.3390/ijms252313098 - 5 Dec 2024
Cited by 3 | Viewed by 3405
Abstract
Brain-derived neurotrophic factor (BDNF) is critical for neuroplasticity, synaptic transmission, and neuronal survival. Studies have implicated it in the pathophysiology of depression, as its expression is significantly reduced in brain areas such as the prefrontal cortex and hippocampus in patients with depression. Our [...] Read more.
Brain-derived neurotrophic factor (BDNF) is critical for neuroplasticity, synaptic transmission, and neuronal survival. Studies have implicated it in the pathophysiology of depression, as its expression is significantly reduced in brain areas such as the prefrontal cortex and hippocampus in patients with depression. Our narrative review focuses on the relationship between BDNF, ketamine, and esketamine, specifically by summarizing human studies investigating BDNF variations in patients treated with these two drugs. BDNF plays a pivotal role in neuroplasticity and neurotrophic mechanisms that can be enhanced by traditional antidepressants, which have been shown to increase BDNF levels both peripherally and in targeted brain regions. Ketamine and its S-enantiomer, esketamine, exert both rapid and sustained antidepressant effects through activation of glutamate-related pathways, with neurotrophic effects involving BDNF, as demonstrated in experimental studies. However, clinical findings have shown mixed results, with most indicating an increase in plasma BDNF in patients treated with intravenous ketamine, although some studies contradict these findings. In addition to this, there are few studies of BDNF and esketamine. Currently, the limited number of studies suggests the need for further research, including larger sample sizes and investigations of BDNF and intranasal esketamine, which has been approved by several regulatory agencies for the treatment of treatment-resistant depression. Full article
(This article belongs to the Special Issue Molecular Insights into Neurotrophins and Neuropsychiatric Disorders)
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20 pages, 1372 KiB  
Review
Advances in the Treatment of Cognitive Impairment in Schizophrenia: Targeting NMDA Receptor Pathways
by Ting Zhang, Chang Liu, Ning Zhong, Yichen Wang, Yiyun Huang and Xiaoqin Zhang
Int. J. Mol. Sci. 2024, 25(19), 10668; https://doi.org/10.3390/ijms251910668 - 3 Oct 2024
Cited by 5 | Viewed by 3304
Abstract
Cognitive impairment is a core feature of schizophrenia, playing a pivotal role in the pathogenesis and prognosis of this disorder. Cognitive impairment in schizophrenia encompasses a wide range of domains, including processing speed, episodic memory, working memory, and executive function. These deficits persist [...] Read more.
Cognitive impairment is a core feature of schizophrenia, playing a pivotal role in the pathogenesis and prognosis of this disorder. Cognitive impairment in schizophrenia encompasses a wide range of domains, including processing speed, episodic memory, working memory, and executive function. These deficits persist throughout the course of the illness and significantly impact functional outcomes and quality of life. Therefore, it is imperative to identify the biological basis of cognitive deficits in schizophrenia and develop effective treatments. The role of N-methyl-D-aspartate (NMDA) receptors in synaptic transmission and plasticity has long been recognized, making them potential targets for schizophrenia treatment. This review will focus on emerging pharmacology targeting NMDA receptors, offering strategies for the prevention and treatment of cognitive deficits in schizophrenia. Full article
(This article belongs to the Special Issue Molecular Insights into Neurotrophins and Neuropsychiatric Disorders)
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21 pages, 1511 KiB  
Review
Psychobiotic Properties of Lactiplantibacillus plantarum in Neurodegenerative Diseases
by Mariagiovanna Di Chiano, Fabio Sallustio, Daniela Fiocco, Maria Teresa Rocchetti, Giuseppe Spano, Paola Pontrelli, Antonio Moschetta, Loreto Gesualdo, Raffaella Maria Gadaleta and Anna Gallone
Int. J. Mol. Sci. 2024, 25(17), 9489; https://doi.org/10.3390/ijms25179489 - 31 Aug 2024
Cited by 3 | Viewed by 3695
Abstract
Neurodegenerative disorders are the main cause of cognitive and physical disabilities, affect millions of people worldwide, and their incidence is on the rise. Emerging evidence pinpoints a disturbance of the communication of the gut–brain axis, and in particular to gut microbial dysbiosis, as [...] Read more.
Neurodegenerative disorders are the main cause of cognitive and physical disabilities, affect millions of people worldwide, and their incidence is on the rise. Emerging evidence pinpoints a disturbance of the communication of the gut–brain axis, and in particular to gut microbial dysbiosis, as one of the contributors to the pathogenesis of these diseases. In fact, dysbiosis has been associated with neuro-inflammatory processes, hyperactivation of the neuronal immune system, impaired cognitive functions, aging, depression, sleeping disorders, and anxiety. With the rapid advance in metagenomics, metabolomics, and big data analysis, together with a multidisciplinary approach, a new horizon has just emerged in the fields of translational neurodegenerative disease. In fact, recent studies focusing on taxonomic profiling and leaky gut in the pathogenesis of neurodegenerative disorders are not only shedding light on an overlooked field but are also creating opportunities for biomarker discovery and development of new therapeutic and adjuvant strategies to treat these disorders. Lactiplantibacillus plantarum (LBP) strains are emerging as promising psychobiotics for the treatment of these diseases. In fact, LBP strains are able to promote eubiosis, increase the enrichment of bacteria producing beneficial metabolites such as short-chain fatty acids, boost the production of neurotransmitters, and support the homeostasis of the gut–brain axis. In this review, we summarize the current knowledge on the role of the gut microbiota in the pathogenesis of neurodegenerative disorders with a particular focus on the benefits of LBP strains in Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, autism, anxiety, and depression. Full article
(This article belongs to the Special Issue Molecular Insights into Neurotrophins and Neuropsychiatric Disorders)
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