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Animal Research Model for Neurological Diseases
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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: 30 June 2024 | Viewed by 2925

Special Issue Editors

Dr. Giuseppe Montalbano

E-Mail Website1 Website2
Guest Editor
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
Dr. Sepand Rastegar

E-Mail Website1 Website2
Guest Editor
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.

Keywords

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

Published Papers (4 papers)

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Research

30 pages, 3860 KiB  
Article
Dolutegravir and Folic Acid Interaction during Neural System Development in Zebrafish Embryos
by Daniela Zizioli, Eugenia Quiros-Roldan, Sara Ferretti, Luca Mignani, Giorgio Tiecco, Eugenio Monti, Francesco Castelli and Isabella Zanella
Int. J. Mol. Sci. 2024, 25(9), 4640; https://doi.org/10.3390/ijms25094640 (registering DOI) - 24 Apr 2024
Viewed by 227
Abstract
Dolutegravir (DTG) is one of the most prescribed antiretroviral drugs for treating people with HIV infection, including women of child-bearing potential or pregnant. Nonetheless, neuropsychiatric symptoms are frequently reported. Early reports suggested that, probably in relation to folic acid (FA) shortage, DTG may [...] Read more.
Dolutegravir (DTG) is one of the most prescribed antiretroviral drugs for treating people with HIV infection, including women of child-bearing potential or pregnant. Nonetheless, neuropsychiatric symptoms are frequently reported. Early reports suggested that, probably in relation to folic acid (FA) shortage, DTG may induce neural tube defects in infants born to women taking the drug during pregnancy. Subsequent reports did not definitively confirm these findings. Recent studies in animal models have highlighted the association between DTG exposure in utero and congenital anomalies, and an increased risk of neurologic abnormalities in children exposed during in utero life has been reported. Underlying mechanisms for DTG-related neurologic symptoms and congenital anomalies are not fully understood. We aimed to deepen our knowledge on the neurodevelopmental effects of DTG exposure and further explore the protective role of FA by the use of zebrafish embryos. We treated embryos at 4 and up to 144 h post fertilization (hpf) with a subtherapeutic DTG concentration (1 μM) and observed the disruption of the anterior–posterior axis and several morphological malformations in the developing brain that were both prevented by pre-exposure (2 hpf) and rescued by post-exposure (10 hpf) with FA. By whole-mount in situ hybridization with riboprobes for genes that are crucial during the early phases of neurodevelopment (ntl, pax2a, ngn1, neurod1) and by in vivo visualization of the transgenic Tg(ngn1:EGFP) zebrafish line, we found that DTG induced severe neurodevelopmental defects over time in most regions of the nervous system (notochord, midbrain–hindbrain boundary, eye, forebrain, midbrain, hindbrain, spinal cord) that were mostly but not completely rescued by FA supplementation. Of note, we observed the disruption of ngn1 expression in the dopaminergic regions of the developing forebrain, spinal cord neurons and spinal motor neuron projections, with the depletion of the tyrosine hydroxylase (TH)+ dopaminergic neurons of the dorsal diencephalon and the strong reduction in larvae locomotion. Our study further supports previous evidence that DTG can interfere with FA pathways in the developing brain but also provides new insights regarding the mechanisms involved in the increased risk of DTG-associated fetal neurodevelopmental defects and adverse neurologic outcomes in in utero exposed children, suggesting the impairment of dopaminergic pathways. Full article
(This article belongs to the Special Issue Animal Research Model for Neurological Diseases)
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11 pages, 1449 KiB  
Article
Rats Selected for Different Nervous Excitability: Long-Term Emotional–Painful Stress Affects the Dynamics of DNA Damage in Cells of Several Brain Areas
by Veronika Shcherbinina, Marina Pavlova, Eugene Daev and Natalia Dyuzhikova
Int. J. Mol. Sci. 2024, 25(2), 994; https://doi.org/10.3390/ijms25020994 - 13 Jan 2024
Viewed by 555
Abstract
The maintenance of genome stability is critical for health, but during individual ontogenesis, different stressors affect DNA integrity, which can lead to functional and/or structural changes in the cells of target organs. In the nervous system, cell genome destabilization is associated with different [...] Read more.
The maintenance of genome stability is critical for health, but during individual ontogenesis, different stressors affect DNA integrity, which can lead to functional and/or structural changes in the cells of target organs. In the nervous system, cell genome destabilization is associated with different neurological and psychiatric diseases, but experiments in vivo, where a link between stress and DNA instability has been demonstrated, are relatively rare. Here, we use rat strains selected for the contrast excitability of the tibialis nerve (n. tibialis) and nonselected Wistar rats to investigate the reasons for individual differences in developing post-stress pathologies. Previous research on the behavioral response of these strains to prolonged emotional–painful stress (PEPS) allows us to consider one strain as a model of post-traumatic stress disorder (PTSD) and another strain as a model of compulsive disorder (CD). We study DNA damage in the cells of the prefrontal cortex (PFC), hippocampus, and amygdala, regions involved in stress responses and the formation of post-stress dysfunctions. The evaluation of cell genome integrity via the comet assay shows different responses to PEPS in each brain area analyzed and for all strains used. This could help us to understand the reasons for individual differences in the consequences of stress and the pathophysiology of post-stress disease formation. Full article
(This article belongs to the Special Issue Animal Research Model for Neurological Diseases)
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15 pages, 6882 KiB  
Article
Swine Pudendal Nerve as a Model for Neuromodulation Studies to Restore Lower Urinary Tract Dysfunction
by Alice Giannotti, Stefania Musco, Vincenzo Miragliotta, Giulia Lazzarini, Andrea Pirone, Angela Briganti, Claudio Verardo, Fabio Bernini, Giulio Del Popolo and Silvestro Micera
Int. J. Mol. Sci. 2024, 25(2), 855; https://doi.org/10.3390/ijms25020855 - 10 Jan 2024
Viewed by 706
Abstract
Lower urinary tract dysfunction, such as incontinence or urinary retention, is one of the leading consequences of neurological diseases. This significantly impacts the quality of life for those affected, with implications extending not only to humans but also to clinical veterinary care. Having [...] Read more.
Lower urinary tract dysfunction, such as incontinence or urinary retention, is one of the leading consequences of neurological diseases. This significantly impacts the quality of life for those affected, with implications extending not only to humans but also to clinical veterinary care. Having motor and sensory fibers, the pudendal nerve is an optimal candidate for neuromodulation therapies using bidirectional intraneural prostheses, paving the way towards the restoration of a more physiological urination cycle: bladder state can be detected from recorded neural signals, then an electrical current can be injected to the nerve based on the real-time need of the bladder. To develop such prostheses and investigate this novel approach, animal studies are still required since the morphology of the target nerve is fundamental to optimizing the prosthesis design. This study aims to describe the porcine pudendal nerve as a model for neuromodulation studies aiming at restoring lower urinary tract dysfunction. Five male farm pigs were involved in the study. First, a surgical procedure to access the porcine pudendal nerve without muscle resection was developed. Then, an intraneural interface was implanted to confirm the presence of fibers innervating the external urethral sphincter by measuring its electromyographic activity. Finally, the morphophysiology of the porcine pudendal nerve at the level of surgical exposure was described by using histological and immunohistochemical characterization. This analysis confirmed the fasciculate nature of the nerve and the presence of mixed fibers with a spatial and functional organization. These achievements pave the way for further pudendal neuromodulation studies by using a clinically relevant animal model with the potential for translating the findings into clinical applications. Full article
(This article belongs to the Special Issue Animal Research Model for Neurological Diseases)
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18 pages, 1384 KiB  
Article
An Adapted GeneSwitch Toolkit for Comparable Cellular and Animal Models: A Proof of Concept in Modeling Charcot-Marie-Tooth Neuropathy
by Laura Morant, Maria-Luise Petrovic-Erfurth and Albena Jordanova
Int. J. Mol. Sci. 2023, 24(22), 16138; https://doi.org/10.3390/ijms242216138 - 09 Nov 2023
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Abstract
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)
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