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Biomedicines
Special Issues
Advanced Research in Neurogenesis
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Advanced Research in Neurogenesis

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 July 2022) | Viewed by 4804

Special Issue Editor

Dr. Praneeti Pathipati

E-Mail Website
Guest Editor
Department of Laboratory Medicine, UCSF, San Francisco, CA, USA
Interests: brain injuries; vascular injuries; trauma; neurogenesis; inflammation

Special Issue Information

Dear Colleagues,

It has been established that the central nervous system (CNS) has a regenerative capacity across all ages and, currently, a comprehensive understanding and the modulation of neurogenic processes for sustainable favorable outcomes is a critical field of interest. The generation of neural precursor cells from adult mammals, for example, may offer useful perspectives for the development of new strategies for the treatment of various CNS disorders from ischemic injuries to degenerative disorders. A complete understanding of neurogenic processes is essential to ensure accurate and targeted therapy so that spatial, temporal, and age-sensitive processes can be leveraged for maximal benefit. Extensive research over the past decade has highlighted the feasibility of modulating neurogenesis using tools, such as supplementation with growth and immune-modulating factors, genetic modulation, electric stimulation, and physical activity. There is also increasing evidence to show equal or enhanced efficacy with supplementary factors, such as extracellular vesicles, drugs, or combinatorial therapy, and this has paved the way for a new wave of understanding about the repair processes as well as disease processes. It is the effort of this Special Issue to bring together some of the latest and advanced research in the field of neurogenesis to cover a broad spectrum of work investigating the cellular and molecular mechanisms underlying the regulation of neurogenic processes and beyond. Original and review articles are welcome.

Dr. Praneeti Pathipati
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

  • neurogenesis
  • gliogenesis
  • neural precursor cells
  • stem cells
  • neurite outgrowth
  • neural connections
  • neurological deficits
  • neurodegeneration

Published Papers (2 papers)

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Research

17 pages, 3237 KiB  
Article
Docosahexaenoic Acid and Melatonin Prevent Impaired Oligodendrogenesis Induced by Intrauterine Growth Restriction (IUGR)
by Britta Anna Kühne, Paula Vázquez-Aristizabal, Mercè Fuentes-Amell, Laura Pla, Carla Loreiro, Jesús Gómez-Catalán, Eduard Gratacós, Miriam Illa and Marta Barenys
Biomedicines 2022, 10(5), 1205; https://doi.org/10.3390/biomedicines10051205 - 23 May 2022
Cited by 3 | Viewed by 2149
Abstract
In this study, our aims were to characterize oligodendrogenesis alterations in fetuses with intrauterine growth restriction (IUGR) and to find therapeutic strategies to prevent/treat them using a novel rabbit in vitro neurosphere culture. IUGR was surgically induced in one uterine horn of pregnant [...] Read more.
In this study, our aims were to characterize oligodendrogenesis alterations in fetuses with intrauterine growth restriction (IUGR) and to find therapeutic strategies to prevent/treat them using a novel rabbit in vitro neurosphere culture. IUGR was surgically induced in one uterine horn of pregnant rabbits, while the contralateral horn served as a control. Neural progenitor cells (NPCs) were obtained from pup’s whole brain and cultured as neurospheres mimicking the basic processes of brain development including migration and cell differentiation. Five substances, chosen based on evidence provided in the literature, were screened in vitro in neurospheres from untreated rabbits: Docosahexaenoic acid (DHA), melatonin (MEL), zinc, 3,3′,5-Triiodo-L-thyronine (T3), and lactoferrin (LF) or its metabolite sialic acid (SA). DHA, MEL and LF were further selected for in vivo administration and subsequent evaluation in the Neurosphere Assay. In the IUGR culture, we observed a significantly reduced percentage of oligodendrocytes (OLs) which correlated with clinical findings indicating white matter injury in IUGR infants. We identified DHA and MEL as the most effective therapies. In all cases, our in vitro rabbit neurosphere assay predicted the outcome of the in vivo administration of the therapies and confirmed the reliability of the model, making it a powerful and consistent tool to select new neuroprotective therapies. Full article
(This article belongs to the Special Issue Advanced Research in Neurogenesis)
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16 pages, 5116 KiB  
Article
BMP4 Exerts Anti-Neurogenic Effect via Inducing Id3 during Aging
by Tingting Li, Hongmei Liu, Dongfang Jiang, Keyan Yang, Jiaqi Shen, Haiping Feng, Sijia Wang, Yuxin Zhang, Yun Wang and Tie-Shan Tang
Biomedicines 2022, 10(5), 1147; https://doi.org/10.3390/biomedicines10051147 - 17 May 2022
Cited by 1 | Viewed by 2283
Abstract
Bone morphogenetic protein (BMP) signaling has been shown to be intimately associated with adult neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ). Adult neurogenesis declines in aging rodents and primates. However, the role of BMP signaling in the age-related neurogenesis decline [...] Read more.
Bone morphogenetic protein (BMP) signaling has been shown to be intimately associated with adult neurogenesis in the subventricular zone (SVZ) and subgranular zone (SGZ). Adult neurogenesis declines in aging rodents and primates. However, the role of BMP signaling in the age-related neurogenesis decline remains elusive and the effect of BMP4 on adult SVZ neurogenesis remains controversial. Here, the expression of BMP4 and its canonical effector phosphorylated-Smad1/5/8 (p-Smad1/5/8) in the murine SVZ and SGZ were found to be increased markedly with age. We identified Id3 as a major target of BMP4 in neuronal stem cells (NSCs) of both neurogenic regions, which exhibited a similar increase during aging. Intracerebroventricular infusion of BMP4 activated Smad1/5/8 phosphorylation and upregulated Id3 expression, which further restrained NeuroD1, leading to attenuated neurogenesis in both neurogenic regions and defective differentiation in the SGZ. Conversely, noggin, a potent inhibitor of BMP4, demonstrated opposing effects. In support of this, BMP4 treatment or lentiviral overexpression of Id3 resulted in decreased NeuroD1 protein levels in NSCs of both neurogenic regions and significantly inhibited neurogenesis. Thus, our findings revealed that the increased BMP4 signaling with age inhibited adult neurogenesis in both SVZ and SGZ, which may be attributed at least in part, to the changes in the Id3-NeuroD1 axis. Full article
(This article belongs to the Special Issue Advanced Research in Neurogenesis)
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