Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.9
5.1
Journals
Cells
Special Issues
Animal Models for the Research of Alzheimer's Disease and Neurodegeneration
share announcement

Animal Models for the Research of Alzheimer's Disease and Neurodegeneration

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: closed (16 August 2023) | Viewed by 2891

Special Issue Editors

Dr. Dongming Cai

E-Mail Website
Guest Editor
Department of Neurology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA
Interests: phospholipids; Alzheimer's disease; mouse models; apolipoprotein; endo-lysosomal pathways; drug development
Special Issues, Collections and Topics in MDPI journals
Dr. Mariana Lemos Duarte

E-Mail Website
Guest Editor
MSSM Department of Neurology, Icahn School of Medicine at Mount Sinai, 1468 Madison Avenue, New York, NY 10029, USA
Interests: Alzheimer's disease; memory; mouse models; human-induced pluripotent stem cells; phospholipids; kinase signaling; molecular pharmacology; tauopathy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is a major healthcare burden with a large patient population. Currently there are no effective therapies to stop or slow down the progression of AD. The major challenge in this field is the lack of a better understanding of AD pathophysiology due to its multifaceted disease mechanisms. Animal models have been widely utilized in AD research to study the pathogenesis of AD and test drug efficacy at pre-clinical stages. In the past decade or so, innovative approaches have been developed including novel animal modeling technologies to better recapitulate pathological changes in AD and neurodegeneration in vivo, and to guide the preclinical development of efficacious therapies for AD.

This Special Issue will examine the currently available mouse models of AD, including both familial and sporadic AD mouse models, as well as other animal models. The development of animal models of AD-related neurodegenerative disorders will be explored as well. The pathological and behavioral phenotypes of various animal models of AD and neurodegenerative disorders will be discussed. The approaches of modeling environmental and genetic risk factors of AD in vivo in animals, as well as the selection of animal modeling for preclinical drug development in AD, will be investigated. 

You may choose our Joint Special Issue in Geriatrics.

Dr. Dongming Cai
Dr. Mariana Lemos Duarte
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. Cells is an international peer-reviewed open access semimonthly 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 2700 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

  • Alzheimer’s disease (AD)
  • animal models
  • disease mechanisms
  • pathological changes
  • behavioral phenotypes
  • environmental factors
  • genetic risk factors
  • drug development

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

26 pages, 3161 KiB  
Article
Levels of Amyloid Beta (Aβ) Expression in the Caenorhabditis elegans Neurons Influence the Onset and Severity of Neuronally Mediated Phenotypes
by Neha Sirwani, Shannon M. Hedtke, Kirsten Grant, Gawain McColl and Warwick N. Grant
Cells 2024, 13(18), 1598; https://doi.org/10.3390/cells13181598 - 23 Sep 2024
Viewed by 1027
Abstract
A characteristic feature of Alzheimer’s disease (AD) is the formation of neuronal extracellular senile plaques composed of aggregates of fibrillar amyloid β (Aβ) peptides, with the Aβ1-42 peptide being the most abundant species. These Aβ peptides have been proposed to contribute [...] Read more.
A characteristic feature of Alzheimer’s disease (AD) is the formation of neuronal extracellular senile plaques composed of aggregates of fibrillar amyloid β (Aβ) peptides, with the Aβ1-42 peptide being the most abundant species. These Aβ peptides have been proposed to contribute to the pathophysiology of the disease; however, there are few tools available to test this hypothesis directly. In particular, there are no data that establish a dose–response relationship between Aβ peptide expression level and disease. We have generated a panel of transgenic Caenorhabditis elegans strains expressing the human Aβ1-42 peptide under the control of promoter regions of two pan-neuronal expressed genes, snb-1 and rgef-1. Phenotypic data show strong age-related defects in motility, subtle changes in chemotaxis, reduced median and maximum lifespan, changes in health span indicators, and impaired learning. The Aβ1-42 expression level of these strains differed as a function of promoter identity and transgene copy number, and the timing and severity of phenotypes mediated by Aβ1-42 were strongly positively correlated with expression level. The pan-neuronal expression of varying levels of human Aβ1-42 in a nematode model provides a new tool to investigate the in vivo toxicity of neuronal Aβ expression and the molecular and cellular mechanisms underlying AD progression in the absence of endogenous Aβ peptides. More importantly, it allows direct quantitative testing of the dose–response relationship between neuronal Aβ peptide expression and disease for the first time. These strains may also be used to develop screens for novel therapeutics to treat Alzheimer’s disease. Full article
(This article belongs to the Special Issue Animal Models for the Research of Alzheimer's Disease and Neurodegeneration)
►▼ Show Figures

Figure 1

21 pages, 5102 KiB  
Article
Alzheimer’s Disease-like Pathological Features in the Dorsal Hippocampus of Wild-Type Rats Subjected to Methionine-Diet-Evoked Mild Hyperhomocysteinaemia
by Maria Kovalska, Petra Hnilicova, Dagmar Kalenska, Marian Adamkov, Libusa Kovalska and Jan Lehotsky
Cells 2023, 12(16), 2087; https://doi.org/10.3390/cells12162087 - 17 Aug 2023
Cited by 2 | Viewed by 1505
Abstract
Multifactorial interactions, including nutritional state, likely participate in neurodegeneration’s pathogenesis and evolution. Dysregulation in methionine (Met) metabolism could lead to the development of hyperhomocysteinaemia (hHcy), playing an important role in neuronal dysfunction, which could potentially lead to the development of Alzheimer’s disease (AD)-like [...] Read more.
Multifactorial interactions, including nutritional state, likely participate in neurodegeneration’s pathogenesis and evolution. Dysregulation in methionine (Met) metabolism could lead to the development of hyperhomocysteinaemia (hHcy), playing an important role in neuronal dysfunction, which could potentially lead to the development of Alzheimer’s disease (AD)-like pathological features. This study combines proton magnetic resonance spectroscopy (1H MRS) with immunohistochemical analysis to examine changes in the metabolic ratio and histomorphological alterations in the dorsal rat hippocampus (dentate gyrus—DG) subjected to a high Met diet. Male Wistar rats (420–480 g) underwent hHcy evoked by a Met-enriched diet (2 g/kg of weight/day) lasting four weeks. Changes in the metabolic ratio profile and significant histomorphological alterations have been found in the DG of hHcy rats. We have detected increased morphologically changed neurons and glial cells with increased neurogenic markers and apolipoprotein E positivity parallel with a diminished immunosignal for the N-Methyl-D-Aspartate receptor 1 in hHcy animals. A Met diet induced hHcy, likely via direct Hcy neurotoxicity, an interference with one carbon unit metabolism, and/or epigenetic regulation. These conditions lead to the progression of neurodegeneration and the promotion of AD-like pathological features in the less vulnerable hippocampal DG, which presents a plausible therapeutic target. Full article
(This article belongs to the Special Issue Animal Models for the Research of Alzheimer's Disease and Neurodegeneration)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop