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Molecular Research in Neurodevelopmental Disorders
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Molecular Research in Neurodevelopmental 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: 31 May 2024 | Viewed by 4603

Special Issue Editor

Prof. Dr. Yi-Chuan Cheng

E-Mail Website
Guest Editor
Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan 33302, Taiwan
Interests: developmental biology; neural development; neurodegerative disorders; brain tumors

Special Issue Information

Dear Colleagues,

Neurodevelopmental disorders are caused by defective development of the nervous system, leading to neural, cognitive, psychological, and motor impairments that result in a broad range of symptoms. The causes for neurodevelopmental disorders are heterogeneous, including genetics, metabolism, inflammation, teratogens, nurture, and the interplay of these factors during prenatal or childhood periods. Recent studies have revealed that abnormal function of molecules and signaling pathways is fundamental for the pathology of neurodevelopmental disorders. Therefore, characterization of the molecular regulations underlying these disorders will help to advance the design for diagnosis and treatment approaches.

In this Special Issue, we seek manuscripts describing in-depth studies on the molecular aspect in neurodevelopmental disorders. This Issue will include, but not be limited to, studies on molecular regulation in different neural cells and in neurodevelopmental processes in spatial and temporal manners that help to understand the mechanisms underlying the pathology of neurodevelopmental disorders. Studies using animal models are specifically encouraged, but in vitro cellular and 3D organoid models are also welcome.

Prof. Dr. Yi-Chuan Cheng
Guest Editor

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

  • neurodevelopmental disorders
  • genetics
  • molecular pathways
  • neural development
  • neurogenesis
  • animal models

Published Papers (3 papers)

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Research

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16 pages, 7651 KiB  
Article
Microcephaly Gene Mcph1 Deficiency Induces p19ARF-Dependent Cell Cycle Arrest and Senescence
by Yi-Nan Jiang, Yizhen Gao, Xianxin Lai, Xinjie Li, Gen Liu, Mingmei Ding, Zhiyi Wang, Zixiang Guo, Yinying Qin, Xin Li, Litao Sun, Zhao-Qi Wang and Zhong-Wei Zhou
Int. J. Mol. Sci. 2024, 25(9), 4597; https://doi.org/10.3390/ijms25094597 - 23 Apr 2024
Viewed by 234
Abstract
MCPH1 has been identified as the causal gene for primary microcephaly type 1, a neurodevelopmental disorder characterized by reduced brain size and delayed growth. As a multifunction protein, MCPH1 has been reported to repress the expression of TERT and interact with transcriptional regulator [...] Read more.
MCPH1 has been identified as the causal gene for primary microcephaly type 1, a neurodevelopmental disorder characterized by reduced brain size and delayed growth. As a multifunction protein, MCPH1 has been reported to repress the expression of TERT and interact with transcriptional regulator E2F1. However, it remains unclear whether MCPH1 regulates brain development through its transcriptional regulation function. This study showed that the knockout of Mcph1 in mice leads to delayed growth as early as the embryo stage E11.5. Transcriptome analysis (RNA-seq) revealed that the deletion of Mcph1 resulted in changes in the expression levels of a limited number of genes. Although the expression of some of E2F1 targets, such as Satb2 and Cdkn1c, was affected, the differentially expressed genes (DEGs) were not significantly enriched as E2F1 target genes. Further investigations showed that primary and immortalized Mcph1 knockout mouse embryonic fibroblasts (MEFs) exhibited cell cycle arrest and cellular senescence phenotype. Interestingly, the upregulation of p19ARF was detected in Mcph1 knockout MEFs, and silencing p19Arf restored the cell cycle and growth arrest to wild-type levels. Our findings suggested it is unlikely that MCPH1 regulates neurodevelopment through E2F1-mediated transcriptional regulation, and p19ARF-dependent cell cycle arrest and cellular senescence may contribute to the developmental abnormalities observed in primary microcephaly. Full article
(This article belongs to the Special Issue Molecular Research in Neurodevelopmental Disorders)
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19 pages, 4772 KiB  
Article
The Dual Roles of Triiodothyronine in Regulating the Morphology of Hair Cells and Supporting Cells during Critical Periods of Mouse Cochlear Development
by Xue Bai, Kai Xu, Le Xie, Yue Qiu, Sen Chen and Yu Sun
Int. J. Mol. Sci. 2023, 24(5), 4559; https://doi.org/10.3390/ijms24054559 - 25 Feb 2023
Viewed by 1504
Abstract
Clinically, thyroid-related diseases such as endemic iodine deficiency and congenital hypothyroidism are associated with hearing loss, suggesting that thyroid hormones are essential for the development of normal hearing. Triiodothyronine (T3) is the main active form of thyroid hormone and its effect on the [...] Read more.
Clinically, thyroid-related diseases such as endemic iodine deficiency and congenital hypothyroidism are associated with hearing loss, suggesting that thyroid hormones are essential for the development of normal hearing. Triiodothyronine (T3) is the main active form of thyroid hormone and its effect on the remodeling of the organ of Corti remain unclear. This study aims to explore the effect and mechanism of T3 on the remodeling of the organ of Corti and supporting cells development during early development. In this study, mice treated with T3 at postnatal (P) day 0 or P1 showed severe hearing loss with disordered stereocilia of the outer hair cells (OHCs) and impaired function of mechanoelectrical transduction of OHCs. In addition, we found that treatment with T3 at P0 or P1 resulted in the overproduction of Deiter-like cells. Compared with the control group, the transcription levels of Sox2 and notch pathway-related genes in the cochlea of the T3 group were significantly downregulated. Furthermore, Sox2-haploinsufficient mice treated with T3 not only showed excess numbers of Deiter-like cells but also a large number of ectopic outer pillar cells (OPCs). Our study provides new evidence for the dual roles of T3 in regulating both hair cells and supporting cell development, suggesting that it is possible to increase the reserve of supporting cells. Full article
(This article belongs to the Special Issue Molecular Research in Neurodevelopmental Disorders)
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Review

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19 pages, 2747 KiB  
Review
Early Steps towards Hearing: Placodes and Sensory Development
by Azel Zine and Bernd Fritzsch
Int. J. Mol. Sci. 2023, 24(8), 6994; https://doi.org/10.3390/ijms24086994 - 10 Apr 2023
Cited by 5 | Viewed by 2406
Abstract
Sensorineural hearing loss is the most prevalent sensory deficit in humans. Most cases of hearing loss are due to the degeneration of key structures of the sensory pathway in the cochlea, such as the sensory hair cells, the primary auditory neurons, and their [...] Read more.
Sensorineural hearing loss is the most prevalent sensory deficit in humans. Most cases of hearing loss are due to the degeneration of key structures of the sensory pathway in the cochlea, such as the sensory hair cells, the primary auditory neurons, and their synaptic connection to the hair cells. Different cell-based strategies to replace damaged inner ear neurosensory tissue aiming at the restoration of regeneration or functional recovery are currently the subject of intensive research. Most of these cell-based treatment approaches require experimental in vitro models that rely on a fine understanding of the earliest morphogenetic steps that underlie the in vivo development of the inner ear since its initial induction from a common otic–epibranchial territory. This knowledge will be applied to various proposed experimental cell replacement strategies to either address the feasibility or identify novel therapeutic options for sensorineural hearing loss. In this review, we describe how ear and epibranchial placode development can be recapitulated by focusing on the cellular transformations that occur as the inner ear is converted from a thickening of the surface ectoderm next to the hindbrain known as the otic placode to an otocyst embedded in the head mesenchyme. Finally, we will highlight otic and epibranchial placode development and morphogenetic events towards progenitors of the inner ear and their neurosensory cell derivatives. Full article
(This article belongs to the Special Issue Molecular Research in Neurodevelopmental Disorders)
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