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Modeling Neurogenesis, Regeneration and Disease from Animal Models

A Special Issue of International Journal of Molecular Sciences (ISSN 1422-0067) belonging to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 30 September 2026 | Viewed by 2060

Editors


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Guest Editor
1. Zebrafish Neuromorphology Lab, Department of Veterinary Sciences, University of Messina, Polo Universitario dell’ Annunziata, 98168 Messina, Italy
2. Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno D’Alcontres 31, 98166 Messina, Italy
Interests: zebrafish; nothobranchius; sensory system; ageing; growth

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Guest Editor
Zebrafish Neuromorphology Lab, Department of Veterinary Sciences, University of Messina, Polo Universitario dell’ Annunziata, 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

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Guest Editor
Institute of Biological and Chemical Systems—Biological Information Processing (IBCS-BIP), Karlsruhe Institute of Technology, 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,

Neurogenesis and neural regeneration are central to nervous system development, plasticity, and repair. These processes are regulated by complex molecular signalling pathways, cellular interactions, and structural changes at both tissue and subcellular levels. Disruptions to these processes contribute to a wide spectrum of conditions, including impaired neurogenesis, failed regeneration, neurodevelopmental syndromes, traumatic injuries, and age-associated diseases.

Animal models have been essential for advancing our understanding of the molecular, cellular, and structural mechanisms governing neurogenesis, neural regeneration, and disease progression. Comparative analyses of conserved and divergent pathways, together with the identification of homologous neural structures and cell types, provide powerful in vivo systems for studying neural function, repair, and pathology.

Recent technological advances integrating molecular biology, omics-based approaches, genome editing, imaging, and computational analysis now allow researchers to directly link molecular changes with cellular architecture, tissue organization, and functional outcomes in both development and disease.

We invite researchers to contribute to this Special Issue, which aims to present research using animal models to investigate the molecular and structural bases of neurogenesis, neural regeneration, and neurological disease. By integrating multidisciplinary approaches, this Special Issue will bridge molecular insights with structural and functional outcomes, strengthening the translational relevance of animal-based neuroscience research.

In this Special Issue, original research articles and reviews are welcome. Contributions may address (but are not limited to) the following:

  • Signalling pathways involved in neural regeneration and repair;
  • Translational insights linking molecular and ultrastructural changes to neurological disorders;
  • Animal models of neurodevelopmental and neurodegenerative diseases;
  • Modelling brain injury, spinal cord injury, and neural repair;
  • Role of inflammation, metabolism, and the microenvironment in neural regeneration.

We look forward to receiving your contributions.

Dr. Kamel Mhalhel
Dr. Giuseppe Montalbano
Dr. Sepand Rastegar
Guest Editors

Manuscript Submission Information

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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-anonymized 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

  • neurogenesis
  • neural regeneration
  • animal models
  • neural stem cells
  • neurodevelopment
  • neurodegeneration
  • molecular mechanisms
  • disease modeling
  • nervous system repair, ultrastructure

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Published Papers (2 papers)

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Review

16 pages, 2302 KB  
Review
The Repair Manual of a Fruit Fly Brain
by Isabella Peetz, Ayelet Blum, Shawn Ahern-Djamali and Grace Boekhoff-Falk
Int. J. Mol. Sci. 2026, 27(15), 6795; https://doi.org/10.3390/ijms27156795 - 29 Jul 2026
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Abstract
The brain is a complex organ; its diverse functions and plasticity correspond with an intricate structure. Integrating sensory inputs with internal physiological states, the brain orchestrates balance, posture, movement, speech, emotions, the creation of memories, and the ability to learn. Whether due to [...] Read more.
The brain is a complex organ; its diverse functions and plasticity correspond with an intricate structure. Integrating sensory inputs with internal physiological states, the brain orchestrates balance, posture, movement, speech, emotions, the creation of memories, and the ability to learn. Whether due to trauma, disease, or stroke, disruptions to brain architecture have long-lasting consequences for a person’s physical, behavioral, emotional, and cognitive health. Comparative studies using model systems to identify meaningful therapies and treatments are critical to elucidate the mechanisms underlying regenerative processes in the brain. This review focuses on the model organism Drosophila melanogaster, which has a large repertoire of available molecular and genetic tools for investigation of neural regeneration. Full article
(This article belongs to the Special Issue Modeling Neurogenesis, Regeneration and Disease from Animal Models)
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23 pages, 3667 KB  
Review
LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis
by Tinkara Korošec, Boris Rogelj and Vera Župunski
Int. J. Mol. Sci. 2026, 27(14), 6244; https://doi.org/10.3390/ijms27146244 - 14 Jul 2026
Viewed by 869
Abstract
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive degeneration of upper and lower motor neurons. While monogenic causes account for a minority of cases, in most cases, ALS is sporadic and likely arises from multilayer interactions of genetic [...] Read more.
Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the progressive degeneration of upper and lower motor neurons. While monogenic causes account for a minority of cases, in most cases, ALS is sporadic and likely arises from multilayer interactions of genetic architecture, aging-associated loss of genome regulation, and inflammatory stress. Long interspersed nuclear element-1 (LINE-1) retrotransposons are endogenous mobile elements that are tightly controlled through various cellular mechanisms under normal conditions. When abnormally active, they are involved in gene inactivation, expression regulation, and genomic instability, leading to cellular processes such as innate immunity and cell death. Here, we present mechanistic links between LINE-1 and ALS. These include evidence that the burden of retrotransposition-competent LINE-1s (RC-L1s) is increased in ALS genomes, positioning RC-L1 load as a candidate contributor to missing heritability in sporadic disease. We also integrate emerging data showing that LINE-1 RNA can be intrinsically toxic independently of new insertions, as it promotes chromatin opening and transcriptional epigenetic noise, particularly when nuclear RNA surveillance pathways fail in TDP-43 pathology. Finally, we review how LINE-1-derived DNA/RNA intermediates can engage innate immune sensors, highlighting the cGAS–STING axis as a plausible route from LINE-1 de-repression to neuroinflammation. Together, these concepts support a model in which genetic RC-L1 load and age-/pathology-driven LINE-1 de-repression converge on nuclear dysfunction and inflammatory amplification, suggesting concrete molecular nodes for therapeutic intervention. Full article
(This article belongs to the Special Issue Modeling Neurogenesis, Regeneration and Disease from Animal Models)
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