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Disorders in Brain Development and Nervous System: Key Molecules and Pathology

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 (20 May 2024) | Viewed by 15645

Special Issue Editor

Prof. Dr. Kazuhiko Nakadate

E-Mail Website
Guest Editor
Department of Functional Morphology, Meiji Pharmaceutical University, Tokyo 204-8588, Japan
Interests: drug discovery; natural products; medicinal chemistry; green tea; HPLC; CLEM
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Brain development is the biological process by which neurons are generated. And this process of neuronal development includes proliferation, differentiation, migration, axonal guidance, synaptogenesis, and neural network formation. Prenatal and postnatal brain development are very important for our later social life. During the prenatal and early postnatal period, brain growth is extremely rapid, and in humans, in just his first eight years after birth, the foundation for future learning and health can be laid. However, it is well known that neurons during this developmental stage respond to a myriad of chemical factors, nutritional status, toxins, infections, and many other factors. In the central nervous system, a myriad of chemical factors have been shown to impair not only neuronal differentiation and development, but also neural circuit formation, normal function and morphogenesis, and the association of neurons and glial cells. On the other hand, our brain continues to develop slowly and reach maturity, after which its function gradually weakens. During these times and throughout our lives, various factors affect the neurons in our brains. In recent years, it has become increasingly clear that changes in lifestyle habits and various environmental changes affect the neurons themselves or neural circuits in the brain.

It is necessary to investigate and elucidate the factors that affect the brain, and to analyze in detail how these factors affect the brain. This special issue of the journal calls for discussion of factors that influence prenatal, postnatal, and mature brain structure and function by many molecular factors, and the pathology of the affected brain.

Prof. Dr. Kazuhiko Nakadate
Guest Editor

Manuscript Submission Information

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Keywords

  • neurogenesis
  • neurotrophic factors
  • synapse formation
  • neuronal circuit formation
  • nutrition
  • specific genes for brain development
  • pathology of the affected brain

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Published Papers (7 papers)

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Editorial

Jump to: Research, Review

4 pages, 159 KiB  
Editorial
Disorders in Brain Development and Nervous System: Key Molecules and Pathology
by Kazuhiko Nakadate and Kiyoharu Kawakami
Int. J. Mol. Sci. 2024, 25(20), 10901; https://doi.org/10.3390/ijms252010901 - 10 Oct 2024
Viewed by 1335
Abstract
Brain development is an extremely complex and essential biological process that begins at the start of life and continues throughout an individual’s lifespan [...] Full article
(This article belongs to the Special Issue Disorders in Brain Development and Nervous System: Key Molecules and Pathology)

Research

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14 pages, 14972 KiB  
Article
Brain-Specific Angiogenesis Inhibitor 3 Is Expressed in the Cochlea and Is Necessary for Hearing Function in Mice
by Chika Saegusa, Wataru Kakegawa, Eriko Miura, Takahiro Aimi, Sachiyo Mogi, Tatsuhiko Harada, Taku Yamashita, Michisuke Yuzaki and Masato Fujioka
Int. J. Mol. Sci. 2023, 24(23), 17092; https://doi.org/10.3390/ijms242317092 - 4 Dec 2023
Cited by 2 | Viewed by 1840
Abstract
Mammalian auditory hair cells transduce sound-evoked traveling waves in the cochlea into nerve stimuli, which are essential for hearing function. Pillar cells located between the inner and outer hair cells are involved in the formation of the tunnel of Corti, which incorporates outer-hair-cell-driven [...] Read more.
Mammalian auditory hair cells transduce sound-evoked traveling waves in the cochlea into nerve stimuli, which are essential for hearing function. Pillar cells located between the inner and outer hair cells are involved in the formation of the tunnel of Corti, which incorporates outer-hair-cell-driven fluid oscillation and basilar membrane movement, leading to the fine-tuned frequency-specific perception of sounds by the inner hair cells. However, the detailed molecular mechanism underlying the development and maintenance of pillar cells remains to be elucidated. In this study, we examined the expression and function of brain-specific angiogenesis inhibitor 3 (Bai3), an adhesion G-protein-coupled receptor, in the cochlea. We found that Bai3 was expressed in hair cells in neonatal mice and pillar cells in adult mice, and, interestingly, Bai3 knockout mice revealed the abnormal formation of pillar cells, with the elevation of the hearing threshold in a frequency-dependent manner. Furthermore, old Bai3 knockout mice showed the degeneration of hair cells and spiral ganglion neurons in the basal turn. The results suggest that Bai3 plays a crucial role in the development and/or maintenance of pillar cells, which, in turn, are necessary for normal hearing function. Our results may contribute to understanding the mechanisms of hearing loss in human patients. Full article
(This article belongs to the Special Issue Disorders in Brain Development and Nervous System: Key Molecules and Pathology)
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17 pages, 3192 KiB  
Article
Neonatal Exposure to Lipopolysaccharide Promotes Neurogenesis of Subventricular Zone Progenitors in the Developing Neocortex of Ferrets
by Kazuhiko Sawada, Shiori Kamiya and Tetsuya Kobayashi
Int. J. Mol. Sci. 2023, 24(19), 14962; https://doi.org/10.3390/ijms241914962 - 6 Oct 2023
Viewed by 1785
Abstract
Lipopolysaccharide (LPS) is a natural agonist of toll-like receptor 4 that serves a role in innate immunity. The current study evaluated the LPS-mediated regulation of neurogenesis in the subventricular zone (SVZ) progenitors, that is, the basal radial glia and intermediate progenitors (IPs), in [...] Read more.
Lipopolysaccharide (LPS) is a natural agonist of toll-like receptor 4 that serves a role in innate immunity. The current study evaluated the LPS-mediated regulation of neurogenesis in the subventricular zone (SVZ) progenitors, that is, the basal radial glia and intermediate progenitors (IPs), in ferrets. Ferret pups were subcutaneously injected with LPS (500 μg/g of body weight) on postnatal days (PDs) 6 and 7. Furthermore, 5-ethynyl-2′-deoxyuridine (EdU) and 5-bromo-2′-deoxyuridine (BrdU) were administered on PDs 5 and 7, respectively, to label the post-proliferative and proliferating cells in the inner SVZ (iSVZ) and outer SVZ (oSVZ). A significantly higher density of BrdU single-labeled proliferating cells was observed in the iSVZ of LPS-exposed ferrets than in controls but not in post-proliferative EdU single-labeled and EdU/BrdU double-labeled self-renewing cells. BrdU single-labeled cells exhibited a lower proportion of Tbr2 immunostaining in LPS-exposed ferrets (22.2%) than in controls (42.6%) and a higher proportion of Ctip2 immunostaining in LPS-exposed ferrets (22.2%) than in controls (8.6%). The present findings revealed that LPS modified the neurogenesis of SVZ progenitors. Neonatal LPS exposure facilitates the proliferation of SVZ progenitors, followed by the differentiation of Tbr2-expressing IPs into Ctip2-expressing immature neurons. Full article
(This article belongs to the Special Issue Disorders in Brain Development and Nervous System: Key Molecules and Pathology)
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14 pages, 1867 KiB  
Article
Effectiveness of Albumin-Fused Thioredoxin against 6-Hydroxydopamine-Induced Neurotoxicity In Vitro
by Okina Sakakibara, Mikako Shimoda, Gaku Yamamoto, Youichirou Higashi, Mayumi Ikeda-Imafuku, Yu Ishima, Masahiro Kawahara and Ken-ichiro Tanaka
Int. J. Mol. Sci. 2023, 24(11), 9758; https://doi.org/10.3390/ijms24119758 - 5 Jun 2023
Cited by 3 | Viewed by 2075
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder caused by oxidative stress-dependent loss of dopaminergic neurons in the substantia nigra and elevated microglial inflammatory responses. Recent studies show that cell loss also occurs in the hypothalamus in PD. However, effective treatments for the disorder [...] Read more.
Parkinson’s disease (PD) is a neurodegenerative disorder caused by oxidative stress-dependent loss of dopaminergic neurons in the substantia nigra and elevated microglial inflammatory responses. Recent studies show that cell loss also occurs in the hypothalamus in PD. However, effective treatments for the disorder are lacking. Thioredoxin is the major protein disulfide reductase in vivo. We previously synthesized an albumin–thioredoxin fusion protein (Alb–Trx), which has a longer plasma half-life than thioredoxin, and reported its effectiveness in the treatment of respiratory and renal diseases. Moreover, we reported that the fusion protein inhibits trace metal-dependent cell death in cerebrovascular dementia. Here, we investigated the effectiveness of Alb–Trx against 6-hydroxydopamine (6-OHDA)-induced neurotoxicity in vitro. Alb–Trx significantly inhibited 6-OHDA-induced neuronal cell death and the integrated stress response. Alb–Trx also markedly inhibited 6-OHDA-induced reactive oxygen species (ROS) production, at a concentration similar to that inhibiting cell death. Exposure to 6-OHDA perturbed the mitogen-activated protein kinase pathway, with increased phosphorylated Jun N-terminal kinase and decreased phosphorylated extracellular signal-regulated kinase levels. Alb–Trx pretreatment ameliorated these changes. Furthermore, Alb–Trx suppressed 6-OHDA-induced neuroinflammatory responses by inhibiting NF-κB activation. These findings suggest that Alb–Trx reduces neuronal cell death and neuroinflammatory responses by ameliorating ROS-mediated disruptions in intracellular signaling pathways. Thus, Alb–Trx may have potential as a novel therapeutic agent for PD. Full article
(This article belongs to the Special Issue Disorders in Brain Development and Nervous System: Key Molecules and Pathology)
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30 pages, 4224 KiB  
Article
Differential Early Mechanistic Frontal Lobe Responses to Choline Chloride and Soy Isoflavones in an Experimental Model of Fetal Alcohol Spectrum Disorder
by Suzanne M. de la Monte, Ming Tong and Busra Delikkaya
Int. J. Mol. Sci. 2023, 24(8), 7595; https://doi.org/10.3390/ijms24087595 - 20 Apr 2023
Cited by 4 | Viewed by 2743
Abstract
Fetal alcohol spectrum disorder (FASD) is the most common preventable cause of neurodevelopmental defects, and white matter is a major target of ethanol neurotoxicity. Therapeutic interventions with choline or dietary soy could potentially supplement public health preventive measures. However, since soy contains abundant [...] Read more.
Fetal alcohol spectrum disorder (FASD) is the most common preventable cause of neurodevelopmental defects, and white matter is a major target of ethanol neurotoxicity. Therapeutic interventions with choline or dietary soy could potentially supplement public health preventive measures. However, since soy contains abundant choline, it would be important to know if its benefits are mediated by choline or isoflavones. We compared early mechanistic responses to choline and the Daidzein+Genistein (D+G) soy isoflavones in an FASD model using frontal lobe tissue to assess oligodendrocyte function and Akt-mTOR signaling. Long Evans rat pups were binge administered 2 g/Kg of ethanol or saline (control) on postnatal days P3 and P5. P7 frontal lobe slice cultures were treated with vehicle (Veh), Choline chloride (Chol; 75 µM), or D+G (1 µM each) for 72 h without further ethanol exposures. The expression levels of myelin oligodendrocyte proteins and stress-related molecules were measured by duplex enzyme-linked immunosorbent assays (ELISAs), and mTOR signaling proteins and phosphoproteins were assessed using 11-plex magnetic bead-based ELISAs. Ethanol’s main short-term effects in Veh-treated cultures were to increase GFAP and relative PTEN phosphorylation and reduce Akt phosphorylation. Chol and D+G significantly modulated the expression of oligodendrocyte myelin proteins and mediators of insulin/IGF-1-Akt-mTOR signaling in both control and ethanol-exposed cultures. In general, the responses were more robust with D+G; the main exception was that RPS6 phosphorylation was significantly increased by Chol and not D+G. The findings suggest that dietary soy, with the benefits of providing complete nutrition together with Choline, could be used to help optimize neurodevelopment in humans at risk for FASD. Full article
(This article belongs to the Special Issue Disorders in Brain Development and Nervous System: Key Molecules and Pathology)
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Review

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21 pages, 3337 KiB  
Review
Neurotrophins and Their Receptors: BDNF’s Role in GABAergic Neurodevelopment and Disease
by Carlos Hernández-del Caño, Natalia Varela-Andrés, Alejandro Cebrián-León and Rubén Deogracias
Int. J. Mol. Sci. 2024, 25(15), 8312; https://doi.org/10.3390/ijms25158312 - 30 Jul 2024
Cited by 5 | Viewed by 2206
Abstract
Neurotrophins and their receptors are distinctly expressed during brain development and play crucial roles in the formation, survival, and function of neurons in the nervous system. Among these molecules, brain-derived neurotrophic factor (BDNF) has garnered significant attention due to its involvement in regulating [...] Read more.
Neurotrophins and their receptors are distinctly expressed during brain development and play crucial roles in the formation, survival, and function of neurons in the nervous system. Among these molecules, brain-derived neurotrophic factor (BDNF) has garnered significant attention due to its involvement in regulating GABAergic system development and function. In this review, we summarize and compare the expression patterns and roles of neurotrophins and their receptors in both the developing and adult brains of rodents, macaques, and humans. Then, we focus on the implications of BDNF in the development and function of GABAergic neurons from the cortex and the striatum, as both the presence of BDNF single nucleotide polymorphisms and disruptions in BDNF levels alter the excitatory/inhibitory balance in the brain. This imbalance has different implications in the pathogenesis of neurodevelopmental diseases like autism spectrum disorder (ASD), Rett syndrome (RTT), and schizophrenia (SCZ). Altogether, evidence shows that neurotrophins, especially BDNF, are essential for the development, maintenance, and function of the brain, and disruptions in their expression or signaling are common mechanisms in the pathophysiology of brain diseases. Full article
(This article belongs to the Special Issue Disorders in Brain Development and Nervous System: Key Molecules and Pathology)
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17 pages, 4733 KiB  
Review
Advanced Techniques Using In Vivo Electroporation to Study the Molecular Mechanisms of Cerebral Development Disorders
by Chen Yang, Atsunori Shitamukai, Shucai Yang and Ayano Kawaguchi
Int. J. Mol. Sci. 2023, 24(18), 14128; https://doi.org/10.3390/ijms241814128 - 15 Sep 2023
Cited by 1 | Viewed by 2557
Abstract
The mammalian cerebral cortex undergoes a strictly regulated developmental process. Detailed in situ visualizations, imaging of these dynamic processes, and in vivo functional gene studies significantly enhance our understanding of brain development and related disorders. This review introduces basic techniques and recent advancements [...] Read more.
The mammalian cerebral cortex undergoes a strictly regulated developmental process. Detailed in situ visualizations, imaging of these dynamic processes, and in vivo functional gene studies significantly enhance our understanding of brain development and related disorders. This review introduces basic techniques and recent advancements in in vivo electroporation for investigating the molecular mechanisms underlying cerebral diseases. In utero electroporation (IUE) is extensively used to visualize and modify these processes, including the forced expression of pathological mutants in human diseases; thus, this method can be used to establish animal disease models. The advent of advanced techniques, such as genome editing, including de novo knockout, knock-in, epigenetic editing, and spatiotemporal gene regulation, has further expanded our list of investigative tools. These tools include the iON expression switch for the precise control of timing and copy numbers of exogenous genes and TEMPO for investigating the temporal effects of genes. We also introduce the iGONAD method, an improved genome editing via oviductal nucleic acid delivery approach, as a novel genome-editing technique that has accelerated brain development exploration. These advanced in vivo electroporation methods are expected to provide valuable insights into pathological conditions associated with human brain disorders. Full article
(This article belongs to the Special Issue Disorders in Brain Development and Nervous System: Key Molecules and Pathology)
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