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Biomedicines
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Application of Animal Models and New Therapeutic Approaches in Neurological...
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Application of Animal Models and New Therapeutic Approaches in Neurological Diseases

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

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 6894

Special Issue Editors

Dr. Ana Carolina Pinheiro Campos

E-Mail Website
Guest Editor
Sunnybrook Health Sciences Centre, Toronto, ON, Canada
Interests: Parkinson’s disease; spinal cord; neuroinflammation
Dr. Daniel Oliveira Martins

E-Mail Website
Guest Editor
Hospital Sírio-Libanês, São Paulo, Brazil
Interests: neurodegenerative disorders; orofacial/trigeminal pain; photobiomodulation

Special Issue Information

Dear Colleagues,

Preclinical models are of utmost importance when attempting to better understand the mechanisms of many diseases with great impact worldwide. Constructing a perfect translational animal model can be challenging. However, revealing new animal models that aim to mimic particular characteristics human diseases, providing an the opportunity to discover new translational models that can further represent the pathology, latency, etiology, symptoms and mechanisms of several neurological diseases, may ultimately shed light on the field of neurology and attenuate the limitations of preclinical trials. Comprehending and validating new therapeutic strategies in this field is pivotal to further improve neurological disease treatment and the quality of life of individuals suffering from treatment resistance.

The aim of this Research Topic is to discover and integrate new, state-of-the-art preclinical models that can contribute to minimize current limitations from the classic animal models available for neurological diseases. Furthermore, new therapeutic strategies aiming to attenuate the symptoms and/or the pathology mechanisms of neurological diseases are also welcome. Evidence from preclinical studies, as well as meta-analyses or reviews assembling firm evidence on this theme, will also contribute to our understanding.

Dr. Ana Carolina Pinheiro Campos
Dr. Daniel Oliveira Martins
Guest Editors

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Keywords

  • preclinical models
  • animal models
  • translational models
  • neuromodulation therapeutic strategies

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Published Papers (3 papers)

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Research

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13 pages, 3193 KiB  
Article
The Neuroprotective Effect of Neural Cell Adhesion Molecule L1 in the Hippocampus of Aged Alzheimer’s Disease Model Mice
by Miljana Aksic, Igor Jakovcevski, Mohammad I. K. Hamad, Vladimir Jakovljevic, Sanja Stankovic and Maja Vulovic
Biomedicines 2024, 12(8), 1726; https://doi.org/10.3390/biomedicines12081726 - 1 Aug 2024
Viewed by 887
Abstract
Alzheimer’s disease (AD) is a severe neurodegenerative disorder and the most common form of dementia, causing the loss of cognitive function. Our previous study has shown, using a doubly mutated mouse model of AD (APP/PS1), that the neural adhesion molecule L1 directly binds [...] Read more.
Alzheimer’s disease (AD) is a severe neurodegenerative disorder and the most common form of dementia, causing the loss of cognitive function. Our previous study has shown, using a doubly mutated mouse model of AD (APP/PS1), that the neural adhesion molecule L1 directly binds amyloid peptides and decreases plaque load and gliosis when injected as an adeno-associated virus construct (AAV-L1) into APP/PS1 mice. In this study, we microinjected AAV-L1, using a Hamilton syringe, directly into the 3-month-old APP/PS1 mouse hippocampus and waited for a year until significant neurodegeneration developed. We stereologically counted the principal neurons and parvalbumin-positive interneurons in the hippocampus, estimated the density of inhibitory synapses around principal cells, and compared the AAV-L1 injection models with control injections of green fluorescent protein (AAV-GFP) and the wild-type hippocampus. Our results show that there is a significant loss of granule cells in the dentate gyrus of the APP/PS1 mice, which was improved by AAV-L1 injection, compared with the AAV-GFP controls (p < 0.05). There is also a generalized loss of parvalbumin-positive interneurons in the hippocampus of APP/PS1 mice, which is ameliorated by AAV-L1 injection, compared with the AAV-GFP controls (p < 0.05). Additionally, AAV-L1 injection promotes the survival of inhibitory synapses around the principal cells compared with AAV-GFP controls in all three hippocampal subfields (p < 0.01). Our results indicate that L1 promotes neuronal survival and protects the synapses in an AD mouse model, which could have therapeutic implications. Full article
(This article belongs to the Special Issue Application of Animal Models and New Therapeutic Approaches in Neurological Diseases)
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17 pages, 6915 KiB  
Article
Investigating the Pathogenic Interplay of Alpha-Synuclein, Tau, and Amyloid Beta in Lewy Body Dementia: Insights from Viral-Mediated Overexpression in Transgenic Mouse Models
by Melina J. Lim, Suelen L. Boschen, Aishe Kurti, Monica Castanedes Casey, Virginia R. Phillips, John D. Fryer, Dennis Dickson, Karen R. Jansen-West, Leonard Petrucelli, Marion Delenclos and Pamela J. McLean
Biomedicines 2023, 11(10), 2863; https://doi.org/10.3390/biomedicines11102863 - 22 Oct 2023
Cited by 2 | Viewed by 2958
Abstract
Lewy body dementia (LBD) is an often misdiagnosed and mistreated neurodegenerative disorder clinically characterized by the emergence of neuropsychiatric symptoms followed by motor impairment. LBD falls within an undefined range between Alzheimer’s disease (AD) and Parkinson’s disease (PD) due to the potential pathogenic [...] Read more.
Lewy body dementia (LBD) is an often misdiagnosed and mistreated neurodegenerative disorder clinically characterized by the emergence of neuropsychiatric symptoms followed by motor impairment. LBD falls within an undefined range between Alzheimer’s disease (AD) and Parkinson’s disease (PD) due to the potential pathogenic synergistic effects of tau, beta-amyloid (Aβ), and alpha-synuclein (αsyn). A lack of reliable and relevant animal models hinders the elucidation of the molecular characteristics and phenotypic consequences of these interactions. Here, the goal was to evaluate whether the viral-mediated overexpression of αsyn in adult hTau and APP/PS1 mice or the overexpression of tau in Line 61 hThy1-αsyn mice resulted in pathology and behavior resembling LBD. The transgenes were injected intravenously via the tail vein using AAV-PHP.eB in 3-month-old hThy1-αsyn, hTau, or APP/PS1 mice that were then aged to 6-, 9-, and 12-months-old for subsequent phenotypic and histological characterization. Although we achieved the widespread expression of αsyn in hTau and tau in hThy1-αsyn mice, no αsyn pathology in hTau mice and only mild tau pathology in hThy1-αsyn mice was observed. Additionally, cognitive, motor, and limbic behavior phenotypes were not affected by overexpression of the transgenes. Furthermore, our APP/PS1 mice experienced premature deaths starting at 3 months post-injection (MPI), therefore precluding further analyses at later time points. An evaluation of the remaining 3-MPI indicated no αsyn pathology or cognitive and motor behavioral changes. Taken together, we conclude that the overexpression of αsyn in hTau and APP/PS1 mice and tau in hThy1-αsyn mice does not recapitulate the behavioral and neuropathological phenotypes observed in LBD. Full article
(This article belongs to the Special Issue Application of Animal Models and New Therapeutic Approaches in Neurological Diseases)
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Review

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23 pages, 1237 KiB  
Review
Rodent Models of Huntington’s Disease: An Overview
by Giulio Nittari, Proshanta Roy, Ilenia Martinelli, Vincenzo Bellitto, Daniele Tomassoni, Enea Traini, Seyed Khosrow Tayebati and Francesco Amenta
Biomedicines 2023, 11(12), 3331; https://doi.org/10.3390/biomedicines11123331 - 16 Dec 2023
Cited by 3 | Viewed by 2632
Abstract
Huntington’s disease (HD) is an autosomal-dominant inherited neurological disorder caused by a genetic mutation in the IT15 gene. This neurodegenerative disorder is caused by a polyglutamine repeat expansion mutation in the widely expressed huntingtin (HTT) protein. HD is characterized by the degeneration of [...] Read more.
Huntington’s disease (HD) is an autosomal-dominant inherited neurological disorder caused by a genetic mutation in the IT15 gene. This neurodegenerative disorder is caused by a polyglutamine repeat expansion mutation in the widely expressed huntingtin (HTT) protein. HD is characterized by the degeneration of basal ganglia neurons and progressive cell death in intrinsic neurons of the striatum, accompanied by dementia and involuntary abnormal choreiform movements. Animal models have been extensively studied and have proven to be extremely valuable for therapeutic target evaluations. They reveal the hallmark of the age-dependent formation of aggregates or inclusions consisting of misfolded proteins. Animal models of HD have provided a therapeutic strategy to treat HD by suppressing mutant HTT (mHTT). Transgenic animal models have significantly increased our understanding of the molecular processes and pathophysiological mechanisms underlying the HD behavioral phenotype. Since effective therapies to cure or interrupt the course of the disease are not yet available, clinical research will have to make use of reliable animal models. This paper reviews the main studies of rodents as HD animal models, highlighting the neurological and behavioral differences between them. The choice of an animal model depends on the specific aspect of the disease to be investigated. Toxin-based models can still be useful, but most experimental hypotheses depend on success in a genetic model, whose choice is determined by the experimental question. There are many animal models showing similar HD symptoms or pathologies. They include chemical-induced HDs and genetic HDs, where cell-free and cell culture, lower organisms (such as yeast, Drosophila, C. elegans, zebrafish), rodents (mice, rats), and non-human primates are involved. These models provide accessible systems to study molecular pathogenesis and test potential treatments. For developing more effective pharmacological treatments, better animal models must be available and used to evaluate the efficacy of drugs. Full article
(This article belongs to the Special Issue Application of Animal Models and New Therapeutic Approaches in Neurological Diseases)
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