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Animal Research Model for Neurological Diseases, 2nd Edition
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Animal Research Model for Neurological Diseases, 2nd Edition

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 January 2025 | Viewed by 1190

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
Special Issues, Collections and Topics in MDPI journals
Dr. Sepand Rastegar

E-Mail Website
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.

As volume 1 of the Special Issue “Animal Research Model for Neurological Diseases” has been successful, we will be exploring this issue further in the International Journal of Molecular Sciences (ISSN 1422-0067, IF 4.9, JCR Category Q1). This second 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

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Published Papers (2 papers)

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Research

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18 pages, 3303 KiB  
Article
Acute Paraoxon-Induced Neurotoxicity in a Mouse Survival Model: Oxidative Stress, Dopaminergic System Alterations and Memory Deficits
by Edurne Urquizu, Selma Paratusic, Júlia Goyenechea, Cristian Gómez-Canela, Berta Fumàs, David Pubill, Demetrio Raldúa, Jordi Camarasa, Elena Escubedo and Raúl López-Arnau
Int. J. Mol. Sci. 2024, 25(22), 12248; https://doi.org/10.3390/ijms252212248 - 14 Nov 2024
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Abstract
The secondary neurotoxicity induced by severe organophosphorus (OP) poisoning, including paraoxon (POX), is associated with cognitive impairments in survivors, who, despite receiving appropriate emergency treatments, may still experience lasting neurological deficits. Thus, the present study provides a survival mouse model of acute and [...] Read more.
The secondary neurotoxicity induced by severe organophosphorus (OP) poisoning, including paraoxon (POX), is associated with cognitive impairments in survivors, who, despite receiving appropriate emergency treatments, may still experience lasting neurological deficits. Thus, the present study provides a survival mouse model of acute and severe POX poisoning to examine secondary neurotoxicity. Swiss CD-1 male mice were injected with POX (4 mg/kg, s.c.) followed by atropine (4 mg/kg, i.p.), pralidoxime (2-PAM; Pyridine-2-aldoxime methochloride) (25 mg/kg, i.p., twice, 1 h apart) and diazepam (5 mg/kg, i.p.), resulting in a survival rate >90% and Racine score of 5–6. Our results demonstrated that the model showed increased lipid peroxidation, downregulation of antioxidant enzymes and astrogliosis in the mouse hippocampus (HP) and prefrontal cortex (PFC), brain areas involved in cognitive functions. Moreover, dopamine (DA) levels were reduced in the hp, but increased in the PFC. Furthermore, the survival mouse model of acute POX intoxication did not exhibit phenotypic manifestations of depression, anxiety or motor incoordination. However, our results demonstrated long-term recognition memory impairments, which are in accordance with the molecular and neurochemical effects observed. In conclusion, this mouse model can aid in researching POX exposure’s effects on memory and developing potential countermeasures against the secondary neurotoxicity induced by severe OP poisoning. Full article
(This article belongs to the Special Issue Animal Research Model for Neurological Diseases, 2nd Edition)
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Review

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27 pages, 4414 KiB  
Review
Nature’s Secret Neuro-Regeneration Pathway in Axolotls, Polychaetes and Planarians for Human Therapeutic Target Pathways
by Nur Izzati Mansor, Tengku Nabilatul Balqis, Mohd Nizam Lani, Kwan Liang Lye, Nor Azlan Nor Muhammad, Wan Iryani Wan Ismail and Shahidee Zainal Abidin
Int. J. Mol. Sci. 2024, 25(22), 11904; https://doi.org/10.3390/ijms252211904 - 6 Nov 2024
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Abstract
Despite significant improvements in the comprehension of neuro-regeneration, restoring nerve injury in humans continues to pose a substantial therapeutic difficulty. In the peripheral nervous system (PNS), the nerve regeneration process after injury relies on Schwann cells. These cells play a crucial role in [...] Read more.
Despite significant improvements in the comprehension of neuro-regeneration, restoring nerve injury in humans continues to pose a substantial therapeutic difficulty. In the peripheral nervous system (PNS), the nerve regeneration process after injury relies on Schwann cells. These cells play a crucial role in regulating and releasing different extracellular matrix proteins, including laminin and fibronectin, which are essential for facilitating nerve regeneration. However, during regeneration, the nerve is required to regenerate for a long distance and, subsequently, loses its capacity to facilitate regeneration during this progression. Meanwhile, it has been noted that nerve regeneration has limited capabilities in the central nervous system (CNS) compared to in the PNS. The CNS contains factors that impede the regeneration of axons following injury to the axons. The presence of glial scar formation results from this unfavourable condition, where glial cells accumulate at the injury site, generating a physical and chemical barrier that hinders the regeneration of neurons. In contrast to humans, several species, such as axolotls, polychaetes, and planarians, possess the ability to regenerate their neural systems following amputation. This ability is based on the vast amount of pluripotent stem cells that have the remarkable capacity to differentiate and develop into any cell within their body. Although humans also possess these cells, their numbers are extremely limited. Examining the molecular pathways exhibited by these organisms has the potential to offer a foundational understanding of the human regeneration process. This review provides a concise overview of the molecular pathways involved in axolotl, polychaete, and planarian neuro-regeneration. It has the potential to offer a new perspective on therapeutic approaches for neuro-regeneration in humans. Full article
(This article belongs to the Special Issue Animal Research Model for Neurological Diseases, 2nd Edition)
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