Animal Models of Neurological Disorders: Where Are We Now? (3rd Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 813

Special Issue Editor


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Guest Editor
Department of Biology, Faculty of Science, University of Ottawa, Ottawa, ON K1N 6N5, Canada
Interests: brain development and regeneration; development of dopamine and GABA neurons; control of gene expression; transgenic models; evolution of developmental mechanisms; zebrafish models of disease including Parkinson's disease
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Special Issue Information

Dear Colleagues,

Animal models are powerful tools for investigating the key principles and underlying mechanisms of diseases and disorders. The use of animal models has allowed us to conduct various types of experiments and interrogate the mechanisms underlying diseases and disorders in manners that are unfeasible and unthinkable to apply to human patients. The usefulness of any animal model depends on various parameters such as predictive validity, symptoms, similarity to human conditions, and tractability. To date, various mammalian and non-mammalian animal models of neurological disorders have been established and characterized. They reflect the genetics, behavioral, and/or electrophysiological phenotypes of human patients.

There are various neurological disorders but, in this Issue, we are mainly focusing on five prominent disorders: Parkinson’s disease, Alzheimer’s disease, epilepsy, Huntington’s disease, and schizophrenia. This Special Issue will provide experimental evidence, updated views, and new treatment strategies regarding these disorders. Critical discussions on the advantages and limitations of animal models used to mirror these neurological disorders are also welcome. This Special Issue will cover original articles and reviews on every aspect of mammalian and non-mammalian animal models of Parkinson’s disease, Alzheimer’s disease, epilepsy, Huntington’s disease, and schizophreniaThis may include (but is not limited to) genetic, pharmacological, chemogenetic (such as DREADDs), and optogenetic models of neurological disorders. In this Issue, we also encourage authors to submit work on rare neurological and developmental disorders which affect the brain, spinal cord, or peripheral nerves.

Moreover, we encourage submissions on novel tools and methods related to animal models of the abovementioned neurological disorders as well. Tools and methods will only be considered if they are novel, well documented, discussed, and have the potential to be useful to the scientific world.

Prof. Dr. Marc Ekker
Guest Editor

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Keywords

  • animal model of neurological disorders
  • Parkinson’s disease
  • Alzheimer’s disease
  • epilepsy
  • seizures
  • Huntington’s disease
  • schizophrenia

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Research

18 pages, 1374 KiB  
Article
TAK-653 Reverses Core Depressive Symptoms in Chronic Stress-Induced Monkey Model
by Ling Li, Zhiting Zhang, Xinhe Liu, Mengni Zhou, Shenglin Wen and Ji Dai
Biomedicines 2025, 13(6), 1389; https://doi.org/10.3390/biomedicines13061389 - 5 Jun 2025
Viewed by 510
Abstract
Background: Major Depressive Disorder represents a prevalent and critical mental health issue that highlights the pressing need for innovative therapeutic solutions. Recent research has identified dysfunction within the glutamate system as a crucial element influencing both the onset and management of depressive symptoms. [...] Read more.
Background: Major Depressive Disorder represents a prevalent and critical mental health issue that highlights the pressing need for innovative therapeutic solutions. Recent research has identified dysfunction within the glutamate system as a crucial element influencing both the onset and management of depressive symptoms. Although TAK-653 is a new positive allosteric modulator of AMPA receptors, its effects have not been rigorously examined in models of depression in primates. Methods: To assess its potential antidepressant properties, a chronic unpredictable mild stress protocol was implemented over 12 weeks to create a monkey model of depression, followed by a two-week treatment period with TAK-653. Results: Behavioral evaluations showed that following stress exposure, the monkeys exhibited reduced motivation for food, increased huddling, diminished movement, and a tendency to remain at the lower levels of their enclosure. They also displayed heightened anxiety in response to external stimuli. Plasma analyses indicated higher levels of cortisol, IL-6, and IL-8 in the stressed monkeys compared to baseline readings, confirming the efficacy of the stress-inducing protocol. Post-treatment with TAK-653 resulted in significant improvements, such as enhanced motivation for food, less huddling behavior, greater activity, and a move towards the upper areas of the enclosure. Additionally, the plasma analysis revealed a marked decrease in cortisol and IL-6 levels, along with an increased expression of BDNF. Conclusions: These findings indicate that TAK-653 effectively alleviates depression-like behaviors in nonhuman primate models, thereby paving the way for a promising new strategy in the treatment of depression. Full article
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