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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: 30 April 2024 | Viewed by 3403

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

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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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

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

Published Papers (2 papers)

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Research

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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
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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
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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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