Animal Models for Neurological Disease Research

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 30 November 2025 | Viewed by 1378

Special Issue Editor


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Guest Editor
Department of Fisheries and Wildlife, Michigan State University, East Lansing, MI 48824, USA
Interests: neurogenesis; gene regulation; comparative genomics; zebrafish; regeneration; CRISPR-Cas editing

Special Issue Information

Dear Colleagues,

With advancements in genetic engineering, imaging, and high-throughput sequencing, animal models have become indispensable tools for unraveling the molecular and cellular mechanisms underlying neurological diseases. From transgenic and knockout models to emerging non-traditional organisms, these systems provide critical insights into neurodegenerative disorders, psychiatric conditions, and neurodevelopmental syndromes.

This Special Issue invites original research articles and reviews that explore the development, validation, and application of animal models in neurological disease research. We welcome studies covering the following:

  • New and established genetic models (e.g., CRISPR/Cas9-based modifications and transgenic organisms);
  • Neurophysiological and behavioral analyses in animal models of disease;
  • Single-cell and omics approaches to studying neurodegeneration and brain function;
  • Comparative insights from non-mammalian models (e.g., zebrafish, lamprey, Drosophila, and C. elegans);
  • Innovative biocomputational approaches for analyzing neurological disease pathways;
  • Gene therapy and pharmacological interventions were tested in animal models.

Short communications presenting preliminary but impactful findings will also be considered. This Special Issue aims to provide a comprehensive overview of current progress in translational neurobiology, highlighting how animal models continue to drive innovation in neurological disease research.

We look forward to your contributions.

Dr. Sreeja Sarasamma
Guest Editor

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Keywords

  • animal models
  • neurological diseases
  • genetic models
  • CRISPR/Cas9
  • transgenic organisms
  • behavioral analysis
  • neurodegeneration
  • single-cell approaches
  • zebrafish
  • lamprey
  • biocomputational approaches
  • gene therapy
  • pharmacological interventions
  • translational neurobiology
  • disease pathways

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Published Papers (2 papers)

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Research

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16 pages, 7453 KB  
Article
Red Nucleus Excitatory Neurons Initiate Directional Motor Movement in Mice
by Chenzhao He, Guibo Qi, Xin He, Wenwei Shao, Chao Ma, Zhangfan Wang, Haochuan Wang, Yuntong Tan, Li Yu, Yongsheng Xie, Song Qin and Liang Chen
Biomedicines 2025, 13(8), 1943; https://doi.org/10.3390/biomedicines13081943 - 8 Aug 2025
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Abstract
Background: The red nucleus (RN) is a phylogenetically conserved structure within the midbrain that is traditionally associated with general motor coordination; however, its specific role in controlling directional movement remains poorly understood. Methods: This study systematically investigates the function and mechanism [...] Read more.
Background: The red nucleus (RN) is a phylogenetically conserved structure within the midbrain that is traditionally associated with general motor coordination; however, its specific role in controlling directional movement remains poorly understood. Methods: This study systematically investigates the function and mechanism of RN neurons in directional movement by combining stereotactic brain injections, fiber photometry recordings, multi-unit in vivo electrophysiological recordings, optogenetic manipulation, and anterograde trans-synaptic tracing. Results: We analyzed mice performing standardized T-maze turning tasks and revealed that anatomically distinct RN neuronal ensembles exhibit direction-selective activity patterns. These neurons demonstrate preferential activation during ipsilateral turning movements, with activity onset consistently occurring after movement initiation. We establish a causal relationship between RN neuronal activity and directional motor control: selective activation of RN glutamatergic neurons facilitates ipsilateral turning, whereas temporally precise inhibition significantly impairs the execution of these movements. Anterograde trans-synaptic tracing using H129 reveals that RN neurons selectively project to spinal interneuron populations responsible for ipsilateral flexion and coordinated limb movements. Conclusions: These findings offer a framework for understanding asymmetric motor control in the brain. This work redefines the RN as a specialized hub within midbrain networks that mediate lateralized movements and offers new avenues for neuromodulatory treatments for neurodegenerative and post-injury motor disorders. Full article
(This article belongs to the Special Issue Animal Models for Neurological Disease Research)
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Review

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22 pages, 1830 KB  
Review
Animal Models for the Study of Neurological Diseases and Their Link to Sleep
by Carmen Rubio, Emiliano González-Sánchez, Ángel Lee, Alexis Ponce-Juárez, Norma Serrano-García and Moisés Rubio-Osornio
Biomedicines 2025, 13(8), 2005; https://doi.org/10.3390/biomedicines13082005 - 18 Aug 2025
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Abstract
Sleep is a vital biological function governed by neuronal networks in the brainstem, hypothalamus, and thalamus. Disruptions in these circuits contribute to the sleep disturbances observed in neurodegenerative disorders, including Parkinson’s disease, epilepsy, Huntington’s disease, and Alzheimer’s disease. Oxidative stress, mitochondrial dysfunction, neuroinflammation, [...] Read more.
Sleep is a vital biological function governed by neuronal networks in the brainstem, hypothalamus, and thalamus. Disruptions in these circuits contribute to the sleep disturbances observed in neurodegenerative disorders, including Parkinson’s disease, epilepsy, Huntington’s disease, and Alzheimer’s disease. Oxidative stress, mitochondrial dysfunction, neuroinflammation, and abnormal protein accumulation adversely affect sleep architecture in these conditions. The interaction among these pathological processes is believed to modify sleep-regulating circuits, consequently worsening clinical symptoms. This review examines the cellular and molecular mechanisms that impair sleep regulation in experimental models of these four disorders, emphasizing how oxidative stress, neuroinflammation and synaptic dysfunction contribute to sleep fragmentation and alterations in rapid eye movement (REM) sleep and slow-wave sleep (SWS) phases. In Parkinson’s disease models (6-OHDA and MPTP), dopaminergic degeneration and damage to sleep-regulating nuclei result in daytime somnolence and disrupted sleep patterns. Epilepsy models (kainate, pentylenetetrazole, and kindling) provoke hyperexcitability and oxidative damage, compromising both REM and SWS. Huntington’s disease models (R6/2 and 3-NP) demonstrate reduced sleep duration, circadian irregularities, and oxidative damage in the hypothalamus and suprachiasmatic nucleus. In Alzheimer’s disease (AD) models (APP/PS1, 3xTg-AD, and Tg2576), early sleep problems include diminished SWS and REM sleep, increased awakenings, and circadian rhythm disruption. These changes correlate with β-amyloid and tau deposition, glial activation, chronic inflammation, and mitochondrial damage in the hypothalamus, hippocampus, and prefrontal cortex. Sleep disturbances across these neurodegenerative disease models share common underlying mechanisms like oxidative stress, neuroinflammation, and mitochondrial dysfunction. Understanding these pathways may reveal therapeutic targets to improve both motor symptoms and sleep quality in neurodegenerative disorders. Full article
(This article belongs to the Special Issue Animal Models for Neurological Disease Research)
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