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Translational Neurobiology: Molecular, Cellular, and Sensory Neuroscience in Human Health...
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Translational Neurobiology: Molecular, Cellular, and Sensory Neuroscience in Human Health and Diseases

A special issue of Diseases (ISSN 2079-9721).

Deadline for manuscript submissions: closed (15 December 2023) | Viewed by 9507

Special Issue Editor

Dr. Christian Barbato

E-Mail Website
Guest Editor
Institute of Biochemistry and Cell Biology (IBBC), National Research Council (CNR), Department of Sense Organs, University Sapienza of Rome, Viale del Policlinico 155, Rome, Italy
Interests: microRNA; RNA-induced silencing complex (RISC); RNAmicroRNA; RNA-binding protein; neurodegenerative disease; Alzheimer’s disease; non-coding RNA; RNA metabolism; cellular and molecular neurobiology; neuroCOVID; SARS-CoV-2; post-COVID-19 syndrome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The neuroscience research addressed the complexity of brain function and dysfunction, opening a new scenario in human disease. Basic and translational investigators explored the interface between basic and clinical neuroscience, underlying the importance of Translational Neurobiology, and potential applications in elucidating, treating and preventing brain disorders. Explorations on molecular, cellular, -omics, genetics, and behavioral profiles in neurological and psychiatric diseases, have translational relevance for health. In addition, sensory neuroscience of visual (seeing), auditory (hearing), tactile (touch), gustatory (taste), and olfactory (smell), vestibular (movement) cut across a broad range of neurological disciplines.

We propose that, the Translational Neurobiology, which encompass original basic, clinical and integrative research, has translational relevance for biomedicine.

The aim of this Special Issue entitled ‘Translational Neurobiology: Molecular, Cellular, and Sensory Neuroscience in Human Health and Diseases’, is to explore the recent progress on Translational Neurobiology, and future directions, in the neurobiology of neurological and psychiatric diseases. Original and review articles from this Special Issue will provide recent molecular, cellular, and translational neuroscience studies that highlight the role of neurobiology in central nervous system disorders.

We invite authors to submit their original research as well as review manuscripts on emerging applied neurobiology on human biology and translational medicine findings and future therapeutic applications, mapping the geography of translational neurobiology in human health and diseases.

Dr. Christian Barbato
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. Diseases 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 1800 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

  • molecular and cellular neurobiology
  • neuropathology
  • neurological diseases
  • neurodegenerative diseases
  • neuropsychiatric diseases
  • neurotherapeutics
  • translational neuroscience

Published Papers (3 papers)

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Review

38 pages, 2526 KiB  
Review
UBE3A: The Role in Autism Spectrum Disorders (ASDs) and a Potential Candidate for Biomarker Studies and Designing Therapeutic Strategies
by Bidisha Roy, Enyonam Amemasor, Suhail Hussain and Kimberly Castro
Diseases 2024, 12(1), 7; https://doi.org/10.3390/diseases12010007 - 27 Dec 2023
Viewed by 1723
Abstract
Published reports from the CDC’s Autism and Development Disabilities Monitoring Networks have shown that an average of 1 in every 44 (2.3%) 8-year-old children were estimated to have ASD in 2018. Many of the ASDs exhibiting varying degrees of autism-like phenotypes have chromosomal [...] Read more.
Published reports from the CDC’s Autism and Development Disabilities Monitoring Networks have shown that an average of 1 in every 44 (2.3%) 8-year-old children were estimated to have ASD in 2018. Many of the ASDs exhibiting varying degrees of autism-like phenotypes have chromosomal anomalies in the Chr15q11–q13 region. Numerous potential candidate genes linked with ASD reside in this chromosomal segment. However, several clinical, in vivo, and in vitro studies selected one gene more frequently than others randomly and unbiasedly. This gene codes for UBE3A or Ubiquitin protein ligase E3A [also known as E6AP ubiquitin-protein ligase (E6AP)], an enzyme involved in the cellular degradation of proteins. This gene has been listed as one of the several genes with a high potential of causing ASD in the Autism Database. The gain of function mutations, triplication, or duplication in the UBE3A gene is also associated with ASDs like Angelman Syndrome (AS) and Dup15q Syndrome. The genetic imprinting of UBE3A in the brain and a preference for neuronal maternal-specific expression are the key features of various ASDs. Since the UBE3A gene is involved in two main important diseases associated with autism-like symptoms, there has been widespread research going on in understanding the link between this gene and autism. Additionally, since no universal methodology or mechanism exists for identifying UBE3A-mediated ASD, it continues to be challenging for neurobiologists, neuroscientists, and clinicians to design therapies or diagnostic tools. In this review, we focus on the structure and functional aspects of the UBE3A protein, discuss the primary relevance of the 15q11–q13 region in the cause of ASDs, and highlight the link between UBE3A and ASD. We try to broaden the knowledge of our readers by elaborating on the possible mechanisms underlying UBE3A-mediated ASDs, emphasizing the usage of UBE3A as a prospective biomarker in the preclinical diagnosis of ASDs and discuss the positive outcomes, advanced developments, and the hurdles in the field of therapeutic strategies against UBE3A-mediated ASDs. This review is novel as it lays a very detailed and comprehensive platform for one of the most important genes associated with diseases showing autistic-like symptoms. Additionally, this review also attempts to lay optimistic feedback on the possible steps for the diagnosis, prevention, and therapy of these UBE3A-mediated ASDs in the upcoming years. Full article
(This article belongs to the Special Issue Translational Neurobiology: Molecular, Cellular, and Sensory Neuroscience in Human Health and Diseases)
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28 pages, 2930 KiB  
Review
WNT-β Catenin Signaling as a Potential Therapeutic Target for Neurodegenerative Diseases: Current Status and Future Perspective
by Kakarla Ramakrishna, Lakshmi Vineela Nalla, Dumala Naresh, Kojja Venkateswarlu, Matte Kasi Viswanadh, Buchi N. Nalluri, Guntupalli Chakravarthy, Sajusha Duguluri, Payal Singh, Sachchida Nand Rai, Ashish Kumar, Veer Singh and Santosh Kumar Singh
Diseases 2023, 11(3), 89; https://doi.org/10.3390/diseases11030089 - 25 Jun 2023
Cited by 23 | Viewed by 3191
Abstract
Wnt/β-catenin (WβC) signaling pathway is an important signaling pathway for the maintenance of cellular homeostasis from the embryonic developmental stages to adulthood. The canonical pathway of WβC signaling is essential for neurogenesis, cell proliferation, and neurogenesis, whereas the noncanonical pathway (WNT/Ca2+ and [...] Read more.
Wnt/β-catenin (WβC) signaling pathway is an important signaling pathway for the maintenance of cellular homeostasis from the embryonic developmental stages to adulthood. The canonical pathway of WβC signaling is essential for neurogenesis, cell proliferation, and neurogenesis, whereas the noncanonical pathway (WNT/Ca2+ and WNT/PCP) is responsible for cell polarity, calcium maintenance, and cell migration. Abnormal regulation of WβC signaling is involved in the pathogenesis of several neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), amyotrophic lateral sclerosis (ALS), multiple sclerosis (MS), and spinal muscular atrophy (SMA). Hence, the alteration of WβC signaling is considered a potential therapeutic target for the treatment of neurodegenerative disease. In the present review, we have used the bibliographical information from PubMed, Google Scholar, and Scopus to address the current prospects of WβC signaling role in the abovementioned neurodegenerative diseases. Full article
(This article belongs to the Special Issue Translational Neurobiology: Molecular, Cellular, and Sensory Neuroscience in Human Health and Diseases)
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17 pages, 2318 KiB  
Review
Post-COVID-19 Anosmia and Therapies: Stay Tuned for New Drugs to Sniff Out
by Gabriele Riccardi, Giovanni Francesco Niccolini, Mario Giuseppe Bellizzi, Marco Fiore, Antonio Minni and Christian Barbato
Diseases 2023, 11(2), 79; https://doi.org/10.3390/diseases11020079 - 27 May 2023
Cited by 6 | Viewed by 3746
Abstract
Background: Anosmia is defined as the complete absence of olfactory function, which can be caused by a variety of causes, with upper respiratory tract infections being among the most frequent causes. Anosmia due to SARS-CoV-2 infection has attracted attention given its main role [...] Read more.
Background: Anosmia is defined as the complete absence of olfactory function, which can be caused by a variety of causes, with upper respiratory tract infections being among the most frequent causes. Anosmia due to SARS-CoV-2 infection has attracted attention given its main role in symptomatology and the social impact of the pandemic. Methods: We conducted systematic research in a clinicaltrials.gov database to evaluate all active clinical trials worldwide regarding drug therapies in adult patients for anosmia following SARS-CoV-2 infection with the intention of identifying the nearby prospects to treat Anosmia. We use the following search terms: “Anosmia” AND “COVID-19” OR “SARS-CoV-2” OR “2019 novel coronavirus”. Results: We found 18 active clinical trials that met our criteria: one phase 1, one phase 1–2, five phases 2, two phases 2–3, three phases 3, and six phases 4 studies were identified. The drug therapies that appear more effective and promising are PEA-LUT and Cerebrolysin. The other interesting drugs are 13-cis-retinoic acid plus aerosolized Vitamin D, dexamethasone, and corticosteroid nasal irrigation. Conclusions: COVID-19 has allowed us to highlight how much anosmia is an important and debilitating symptom for patients and, above all, to direct research to find a therapy aimed at curing the symptom, whether it derives from SARS-CoV-2 infection or other infections of the upper airways. Some of these therapies are very promising and are almost at the end of experimentation. They also provide hope in this field, which not addressed until recently. Full article
(This article belongs to the Special Issue Translational Neurobiology: Molecular, Cellular, and Sensory Neuroscience in Human Health and Diseases)
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