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The Language of Neural Cells: Decoding Molecular Signaling in Neurodevelopmental...
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The Language of Neural Cells: Decoding Molecular Signaling in Neurodevelopmental and Neuro-Oncological Disorders

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

Deadline for manuscript submissions: 31 July 2026 | Viewed by 1654

Special Issue Editors

Dr. Marilena Briglia

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Guest Editor
Department of Medicine and Surgery “Kore”, University of Enna, 94100 Enna, Italy
Interests: cell biology; cellular death; eryptosis; molecular signaling pathways; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Dr. Alice Foti

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Guest Editor
Department of Medicine and Surgery, University of Enna “Kore”, 94100 Enna, Italy
Interests: cell biology; biochemical pathways; rare tumors; molecular signaling pathways; nanomedicine
Dr. Adriana C. E. Graziano

E-Mail Website
Guest Editor
Department of Medicine and Surgery, University of Enna “Kore”, 94100 Enna, Italy
Interests: cell biology; neurodegenerative pathways; molecular signaling pathways
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cells communicate through a sophisticated molecular language comprising signaling pathways that regulate vital processes such as growth, differentiation, disease progression and death. In the nervous system, this molecular dialogue is particularly intricate and tightly regulated, as it orchestrates brain development, synaptic plasticity, and the response to injury. In neurodevelopmental and neuro-oncological disorders, however, this language is often distorted. Mutations, epigenetic modifications, and the aberrant expression of signaling components can alter cellular communication, leading to disrupted development, uncontrolled proliferation, or neurodegeneration.

This Special Issue, "The Language of Neural Cells: Decoding Molecular Signaling in Neurodevelopmental and Neuro-Oncological Disorders", aims to explore the dysregulation of signaling pathways specifically in the context of complex disorders of the nervous system, including rare ones.

We invite original research articles, reviews, and perspectives that reveal the molecular mechanisms that contribute to resistance, and how targeted interventions can repair the altered cellular communication for better therapeutic outcomes. Topics may include, but are not limited to, receptor-mediated signaling in neural cells, transcriptional dysregulation in neurodevelopment and neurodegeneration, molecular mechanisms of resistance in CNS tumors, apoptosis induction, epigenetic regulation, and the therapeutic modulation of signaling networks.

Dr. Marilena Briglia
Dr. Alice Foti
Dr. Adriana C. E. Graziano
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 250 words) can be sent to the Editorial Office for assessment.

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

  • neural cells
  • molecular signaling
  • neurodevelopmental disorders
  • neuro-oncological disorders
  • transcriptional dysregulation

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Published Papers (2 papers)

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16 pages, 8468 KB  
Article
Loss of the DCHS1 Intracellular Domain Expands Neurogenic Proliferation and Generates Van Maldergem-like Neurodevelopmental Defects
by Kathryn Byerly, Cayla Wolfe, Magdalena Brei, Hannah Parris, Savannah Fisher, Aimee Alston, Hanmei Dong, Peng Chen, Hai Yao, Fulei Tang, Jan Guz, Sarah Dooley, Taylor Nelson, Brian Loizzi, Ranan Phookan, Cortney Gensemer, Sunil Patel and Russell A. Norris
Cells 2026, 15(7), 587; https://doi.org/10.3390/cells15070587 - 26 Mar 2026
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Abstract
Van Maldergem Syndrome (VMS) is a rare autosomal recessive disorder caused by pathogenic variants in the atypical cadherin genes DCHS1 or FAT4 and is marked by craniofacial, skeletal, and neurodevelopmental abnormalities. Although DCHS1–FAT4 binding is mediated by their respective extracellular domains, the in [...] Read more.
Van Maldergem Syndrome (VMS) is a rare autosomal recessive disorder caused by pathogenic variants in the atypical cadherin genes DCHS1 or FAT4 and is marked by craniofacial, skeletal, and neurodevelopmental abnormalities. Although DCHS1–FAT4 binding is mediated by their respective extracellular domains, the in vivo function of the DCHS1 intracellular domain (ICD) is poorly defined. To test its function, we generated mice in which the DCHS1 ICD was deleted and replaced with a V5 epitope tag (Dchs1ΔICD-V5). Homozygous Dchs1ΔICD-V5/ΔICD-V5 mice are viable but exhibit VMS-like craniofacial flattening with enlarged fontanelles and reduced palatine/maxillary structures, along with airway cartilage abnormalities including reduced mineralization and decreased tracheal circularity. In periventricular regions, wild-type DCHS1 expression shows polarized localization, whereas mice with the ICD deletion exhibit altered cell polarization within the subventricular zone, concomitant with changes in neural cellular distribution. Neonatal brains display reduced pYAP1: YAP1 ratios and increased Ki67+ proliferation with greater Ki67–neuronal co-localization within the periventricular zone. Together, these data identify the DCHS1 ICD as a critical effector for DCHS1 signaling and a regulator of polarity-dependent growth, with associated changes in Hippo pathway activity during craniofacial and neural morphogenesis. Additionally, our data establish Dchs1ΔICD-V5/ΔICD-V5 mice as a model that recapitulates core features of VMS, thereby allowing new mechanistic discoveries into its pathogenesis. Full article
(This article belongs to the Special Issue The Language of Neural Cells: Decoding Molecular Signaling in Neurodevelopmental and Neuro-Oncological Disorders)
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20 pages, 1355 KB  
Systematic Review
Early-Life Microbiota Modulation and Neurodevelopment in Infants: A Systematic Review and Meta-Analysis of Randomized Controlled Trials
by Salvatore Michele Carnazzo, Fabio Allia, Alice Foti, Marilena Briglia, Marcello Maida, Adriana Carol Eleonora Graziano and Andrea Domenico Praticò
Cells 2026, 15(7), 638; https://doi.org/10.3390/cells15070638 - 1 Apr 2026
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Abstract
Changes in microbial composition during early infancy by various factors (mode of delivery, nutritional practices, antibiotic usage, and environmental influences) have been correlated with observable variances in cognitive abilities, temperament, stress response, and the predisposition to neurodevelopmental disorders. Consequently, microbiota-targeted interventions such as [...] Read more.
Changes in microbial composition during early infancy by various factors (mode of delivery, nutritional practices, antibiotic usage, and environmental influences) have been correlated with observable variances in cognitive abilities, temperament, stress response, and the predisposition to neurodevelopmental disorders. Consequently, microbiota-targeted interventions such as probiotics, prebiotics, and synbiotics are being explored as avenues to enrich beneficial microbial taxa, enhance short-chain fatty acid production, fortify mucosal immunity, and mitigate inflammatory responses during these critical periods. Preclinical research, primarily in experimental animal models, has demonstrated a causal link between microbiota composition and developmental processes such as myelination, synaptic plasticity, and socio-emotional behaviors, whereas human evidence remains largely associative and heterogeneous. A notable gap exists in the current literature, which typically centers on gastrointestinal, psychiatric, or preterm outcomes, without a focused investigation into neurodevelopmental assessments within the first three years. To bridge this gap, we conducted a systematic review and meta-analysis of randomized controlled trials assessing the impact of probiotics, prebiotics, and synbiotics on neurodevelopment and behavior in infants aged 0–36 months. Our primary objective was to establish whether microbiota-targeted strategies confer discernible neurodevelopmental benefits, alongside elucidating the mechanisms underpinning the relationship between microbial modulation and early brain development. Full article
(This article belongs to the Special Issue The Language of Neural Cells: Decoding Molecular Signaling in Neurodevelopmental and Neuro-Oncological Disorders)
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