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Cells
Special Issues
Neuronal Development and Disease: From Molecular Bases to Neurological Disorders
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Neuronal Development and Disease: From Molecular Bases to Neurological Disorders

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 1551

Special Issue Editor

Dr. Ramiro Almeida

E-Mail Website
Guest Editor
1. Department of Medical Sciences Institute of Biomedicine—iBiMED, University of Aveiro, Aveiro, Portugal
2. Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal
Interests: synapse formation; local mRNA translation; local protein synthesis; neuronal cell death; excitotoxicity; neurodevelopmental disorders; microfluidics

Special Issue Information

Dear Colleague,

The intricate processes underlying neuronal development are critical in the establishment of a functional nervous system. From early neurogenesis to synaptic formation, these processes are finely tuned, allowing for the proper wiring and functioning of the brain. However, disruptions in these developmental pathways can lead to a wide array of neurological disorders, ranging from developmental disorders in childhood to neurodegenerative diseases in adulthood. Understanding the molecular, genetic, and cellular mechanisms that govern neuronal development and how these mechanisms are altered in disease is crucial in advancing therapeutic strategies.

This Special Issue on neuronal development and disease will bring together cutting-edge research that explores the intersection of these two key domains. Contributions from diverse areas, including stem cell biology, neurogenesis, synaptic plasticity, and neuroinflammation, will provide new insights into the developmental origins of neurological diseases. By including studies on topics spanning model organisms, advanced imaging techniques, and innovative therapeutic approaches, we aim to highlight the complexity of neuronal development and its disruption in disease contexts.

For this Special Issue, we welcome submissions of original research articles and reviews focusing on the mechanisms that explain the regular functioning of the nervous system, as wells as its functioning in disease states, at the cellular, system, or whole-organism level.

Dr. Ramiro Almeida
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • neuronal development
  • neurological disorders
  • neurogenesis
  • neuroinflammation
  • synaptic plasticity

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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22 pages, 3308 KiB  
Article
Epigenetic Reprogramming of Cell Identity in the Rat Primary Neuron–Glia Cultures Involves Histone Serotonylation
by Anastasia A. Borodinova, Yulia A. Leontovich, Alexander P. Beletskiy, Alexander V. Revishchin, Galina V. Pavlova and Pavel M. Balaban
Cells 2025, 14(12), 905; https://doi.org/10.3390/cells14120905 - 15 Jun 2025
Viewed by 408
Abstract
Epigenetic rearrangements can create a favorable environment for the intrinsic plasticity of brain cells, leading to cellular reprogramming into virtually any cell type through the induction of cell-specific transcriptional programs. In this study, we assessed how chromatin remodeling induced by broad-spectrum HDAC inhibitors [...] Read more.
Epigenetic rearrangements can create a favorable environment for the intrinsic plasticity of brain cells, leading to cellular reprogramming into virtually any cell type through the induction of cell-specific transcriptional programs. In this study, we assessed how chromatin remodeling induced by broad-spectrum HDAC inhibitors affects cellular differentiation trajectories in rat primary neuron–glia cultures using a combination of transcriptomics, qPCR, and cytochemistry. We described the epigenetic regulation of transcriptional programs controlled by master transcription factors and neurotrophins in the context of neuronal and glial differentiation and evaluated the expression of representative cell-specific markers. The results obtained suggest that HDAC inhibitors reduce the proliferative potential of cultured cells and induce transcriptomic changes associated with cell differentiation and specialization. Particularly, we revealed a significant upregulation of genes typically expressed in neuromodulatory neurons and the downregulation of genes expressed in glia and inhibitory neurons. Transcriptional changes were accompanied by continuous elevation of histone serotonylation levels in both neurons and glia. Emerging shortly after HDAC inhibition, a complex chromatin remodeling, which includes histone serotonylation, persists over many hours in distinct brain cells. We assume that this sustained epigenetic mechanism likely helps to maintain transcriptional changes associated with cell fate commitment, possibly priming cells for long-term fate conversion. Full article
(This article belongs to the Special Issue Neuronal Development and Disease: From Molecular Bases to Neurological Disorders)
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15 pages, 2592 KiB  
Article
Neuroprotection by Mitochondrial NAD Against Glutamate-Induced Excitotoxicity
by Bruna S. Paiva, Diogo Neves, Diogo Tomé, Filipa J. Costa, Inês C. Bruno, Diogo Trigo, Raquel M. Silva and Ramiro D. Almeida
Cells 2025, 14(8), 582; https://doi.org/10.3390/cells14080582 - 12 Apr 2025
Viewed by 923
Abstract
Excitotoxicity is a pathological process that occurs in many neurological diseases, such as stroke or epilepsy, and is characterized by the extracellular accumulation of high concentrations of glutamate or other excitatory amino acids (EAAs). Nicotinamide adenine dinucleotide (NAD) depletion is an early event [...] Read more.
Excitotoxicity is a pathological process that occurs in many neurological diseases, such as stroke or epilepsy, and is characterized by the extracellular accumulation of high concentrations of glutamate or other excitatory amino acids (EAAs). Nicotinamide adenine dinucleotide (NAD) depletion is an early event following excitotoxicity in many in vitro and in vivo excitotoxic-related models and contributes to the deregulation of energy homeostasis. However, the interplay between glutamate excitotoxicity and the NAD biosynthetic pathway is not fully understood. To address this question, we used a primary culture of rat cortical neurons and found that an excitotoxic glutamate insult alters the expression of the NAD biosynthetic enzymes. Additionally, using a fluorescent NAD mitochondrial sensor, we observed that glutamate induces a significant decrease in the mitochondrial NAD pool, which was reversed when exogenous NAD was added. We also show that exogenous NAD protects against the glutamate-induced decrease in mitochondrial membrane potential (MMP). Glutamate excitotoxicity changed mitochondrial retrograde transport in neurites, which seems to be reversed by NAD addition. Finally, we show that NAD and NAD precursors protect against glutamate-induced cell death. Together, our results demonstrate that glutamate-induced excitotoxicity acts by compromising the NAD biosynthetic pathway, particularly in the mitochondria. These results also uncover a potential role for mitochondrial NAD as a tool for central nervous system (CNS) regenerative therapies. Full article
(This article belongs to the Special Issue Neuronal Development and Disease: From Molecular Bases to Neurological Disorders)
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