Journal Browser

Journal Browser

Special Issue "Animal Research Model for Neurological Diseases"

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 December 2023 | Viewed by 664

Special Issue Editors

Department of Veterinary Sciences, University of Messina, Via Palatucci s.n., Annunziata Universitary Pole, 98168 Messina, Italy
Interests: morphometry; veterinary anatomy; zebrafish; imaging; experimental model; natural compounds; obesity; immunohistochemistry; molecular biology; sensory system; regeneration of sensory cells
Institute of Biological and Chemical Systems-Biological Information Processing (IBCS-BIP), Karlsruhe Institute of Technology (KIT), Postfach 3640, 76021 Karlsruhe, Germany
Interests: gene regulation; transcription; neurogenesis; zebrafish; regeneration; neural stem cell
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Animal modeling of human disease has a fundamental role in scientific studies aimed at explaining disease mechanisms and conducting pre-clinical studies on potential therapies. The careful selection of experimental models for complex pathologies, such as neurological diseases, becomes crucial for ensuring high-quality research outcomes. Consequently, the progress made in animal modeling and the introduction of new models in recent years have significantly contributed to our improved understanding of the principal disease mechanisms of the central nervous system. Numerous aquatic or terrestrial vertebrates, including wild type, transgenic, and mutant models, have been introduced over the past few decades. While the mouse model remains pivotal in central nervous system pathology research, other models such as the zebrafish have also demonstrated remarkable success. This Special Issue aims to explore the morpho-physiopathology and molecular pathways involved in neurological disorders, utilizing both established canonical models and emerging animal models. We invite submissions of full research articles and comprehensive review papers for this Special Issue. This Special Issue is assisted by our Topical Advisory Panel Member Dr. Kamel Mhalhel.

Dr. Giuseppe Montalbano
Dr. Sepand Rastegar
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 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.


  • experimental models
  • mouse
  • rat
  • zebrafish
  • neurological Disease
  • Alzheimer’s disease
  • Parkinson’s disease
  • neurodegeneration
  • neuroregeneration

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:


18 pages, 1384 KiB  
An Adapted GeneSwitch Toolkit for Comparable Cellular and Animal Models: A Proof of Concept in Modeling Charcot-Marie-Tooth Neuropathy
Int. J. Mol. Sci. 2023, 24(22), 16138; https://doi.org/10.3390/ijms242216138 - 09 Nov 2023
Viewed by 412
Investigating the impact of disease-causing mutations, their affected pathways, and/or potential therapeutic strategies using disease modeling often requires the generation of different in vivo and in cellulo models. To date, several approaches have been established to induce transgene expression in a controlled manner [...] Read more.
Investigating the impact of disease-causing mutations, their affected pathways, and/or potential therapeutic strategies using disease modeling often requires the generation of different in vivo and in cellulo models. To date, several approaches have been established to induce transgene expression in a controlled manner in different model systems. Several rounds of subcloning are, however, required, depending on the model organism used, thus bringing labor-intensive experiments into the technical approach and analysis comparison. The GeneSwitch™ technology is an adapted version of the classical UAS-GAL4 inducible system, allowing the spatial and temporal modulation of transgene expression. It consists of three components: a plasmid encoding for the chimeric regulatory pSwitch protein, Mifepristone as an inducer, and an inducible plasmid. While the pSwitch-containing first plasmid can be used both in vivo and in cellulo, the inducible second plasmid can only be used in cellulo. This requires a specific subcloning strategy of the inducible plasmid tailored to the model organism used. To avoid this step and unify gene expression in the transgenic models generated, we replaced the backbone vector with standard pUAS-attB plasmid for both plasmids containing either the chimeric GeneSwitch™ cDNA sequence or the transgene cDNA sequence. We optimized this adapted system to regulate transgene expression in several mammalian cell lines. Moreover, we took advantage of this new system to generate unified cellular and fruit fly models for YARS1-induced Charco–Marie–Tooth neuropathy (CMT). These new models displayed the expected CMT-like phenotypes. In the N2a neuroblastoma cells expressing YARS1 transgenes, we observed the typical “teardrop” distribution of the synthetase that was perturbed when expressing the YARS1CMT mutation. In flies, the ubiquitous expression of YARS1CMT induced dose-dependent developmental lethality and pan-neuronal expression caused locomotor deficit, while expression of the wild-type allele was harmless. Our proof-of-concept disease modeling studies support the efficacy of the adapted transgenesis system as a powerful tool allowing the design of studies with optimal data comparability. Full article
(This article belongs to the Special Issue Animal Research Model for Neurological Diseases)
Show Figures

Figure 1

Back to TopTop