Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
6.0
Journals
Cells
Special Issues
Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies
share announcement

Special Issue "Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies"

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

Deadline for manuscript submissions: 25 February 2024 | Viewed by 10122

Special Issue Editors

Dr. Ines Moreno-Gonzalez

E-Mail Website
Guest Editor
1. Department of Cell Biology, Faculty of Sciences, University of Malaga, IBIMA, 29010 Malaga, Spain
2. Networking Research Center on Neurodegenerative Diseases (CIBERNED), 29010 Malaga, Spain
3. Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston (UTHealth), Houston, TX 77030, USA
Interests: Alzheimer's disease; neurodegeneratrive diseases; amyloid beta; tau; neuroinflammation; risk factors; transgenic animals; preclinical trials
Dr. Claudia Duran-Aniotz

E-Mail Website
Guest Editor
Latin American Brain Health Institute (BrainLat), Center for Social and Cognitive Neuroscience (CSCN), Universidad Adolfo Ibanez, Santiago 7941169, Chile
Interests: biomarkers; dementia; neurodegeneration; Tau; amyloid
Dr. Joana A. Loureiro

E-Mail Website1 Website2
Guest Editor
1. LEPABE - Laboratory for Process Engineering, Environment, Biotechnology and Energy, R. Dr. Roberto Frias, 4200-465 Porto, Portugal
2. ALiCE—Associate Laboratory in Chemical Engineering, Faculty of Engineering, University of Porto, Rua Dr. Roberto Frias, 4200-465 Porto, Portugal
Interests: nanotechnology and interfacial phenomena; effects of fluorinated systems and peptides on the aggregation of amyloid beta peptides; conformational studies of protein and peptide self-organized systems and polymer surfaces; design and production of inorganic and polymeric nanosystems for pharmaceutical and food applications
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer's disease (AD) is the most common form of dementia that accounts for around 50 million cases worldwide. Increasing life expectancy will triple this number by 2050. As long as we remain unable to reverse or prevent AD, its clinical, social, and economic burden will steadily increase hopelessly. The majority of AD cases are sporadic, indicating that the molecular mechanisms that trigger the late onset of the disease are still unknown. Currently, there is no definitive cure for AD, and current clinical interventions help to palliate some clinical symptoms. Prevention and modification of potential risk factors may reduce the probability of developing this type of dementia, but new and more effective therapeutic strategies are needed to prevent, slow down, or even halt the progression of the disease. This Special Issue aims to shed light on the recently described molecular mechanisms that are involved in Alzheimer's pathology, as well as collecting the latest advances in therapeutic interventions to combat this devastating condition.

Dr. Ines Moreno-Gonzalez
Dr. Claudia Duran-Aniotz
Prof. Dr. Joana A. Loureiro
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
  • neurodegeneration
  • risk factors
  • therapy

Published Papers (4 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

Jump to: Review

14 pages, 1830 KiB  
Article
Altering Brain Amyloidosis by Intra-Lingual and Extra-Nasal Exposure of Aβ Aggregates
by
Nazaret Gamez
,
Javiera Bravo-Alegria
,
Yumeng Huang
,
Nelson Perez-Urrutia
,
Deepa Dongarwar
,
Claudio Soto
and
Rodrigo Morales
Cells 2022, 11(21), 3442; https://doi.org/10.3390/cells11213442 - 31 Oct 2022
Viewed by 1281
Abstract
Extensive experimental and human-derived evidence suggest that misfolded Aβ particles spread similarly to infectious prions. Moreover, peripheral administration of Aβ seeds accelerates brain amyloidosis in both susceptible experimental animals and humans. The mechanisms and elements governing the transport of misfolded Aβ from the [...] Read more.
Extensive experimental and human-derived evidence suggest that misfolded Aβ particles spread similarly to infectious prions. Moreover, peripheral administration of Aβ seeds accelerates brain amyloidosis in both susceptible experimental animals and humans. The mechanisms and elements governing the transport of misfolded Aβ from the periphery to the brain are not fully understood, although circulation and retrograde axonal transport have been proposed. Here, we demonstrate that injection of Aβ seeds in the tongue, a highly innervated organ, substantially accelerates the appearance of plaques in Tg2576 mice. In addition, the extra-nasal exposure of Aβ aggregates increased amyloid pathology in the olfactory bulb. Our results show that exposing highly innervated tissues to Aβ seeds accelerates AD-like pathological features, and suggest that Aβ seeds can be transported from peripheral compartments to the brain by retrograde axonal transport. Research in this direction may be relevant on different fronts, including disease mechanisms, diagnosis, and risk-evaluation of potential iatrogenic transmission of Aβ misfolding. Full article
(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)
►▼ Show Figures

Figure 1

13 pages, 1429 KiB  
Article
A Method for Bridging Population-Specific Genotypes to Detect Gene Modules Associated with Alzheimer’s Disease
by
Yulin Dai
,
Peilin Jia
,
Zhongming Zhao
and
Assaf Gottlieb
Cells 2022, 11(14), 2219; https://doi.org/10.3390/cells11142219 - 16 Jul 2022
Cited by 1 | Viewed by 1555
Abstract
Background: Genome-wide association studies have successfully identified variants associated with multiple conditions. However, generalizing discoveries across diverse populations remains challenging due to large variations in genetic composition. Methods that perform gene expression imputation have attempted to address the transferability of gene discoveries across [...] Read more.
Background: Genome-wide association studies have successfully identified variants associated with multiple conditions. However, generalizing discoveries across diverse populations remains challenging due to large variations in genetic composition. Methods that perform gene expression imputation have attempted to address the transferability of gene discoveries across populations, but with limited success. Methods: Here, we introduce a pipeline that combines gene expression imputation with gene module discovery, including a dense gene module search and a gene set variation analysis, to address the transferability issue. Our method feeds association probabilities of imputed gene expression with a selected phenotype into tissue-specific gene-module discovery over protein interaction networks to create higher-level gene modules. Results: We demonstrate our method’s utility in three case-control studies of Alzheimer’s disease (AD) for three different race/ethnic populations (Whites, African descent and Hispanics). We discovered 182 AD-associated genes from gene modules shared between these populations, highlighting new gene modules associated with AD. Conclusions: Our innovative framework has the potential to identify robust discoveries across populations based on gene modules, as demonstrated in AD. Full article
(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)
►▼ Show Figures

Figure 1

14 pages, 989 KiB  
Article
Cerebrospinal Fluid Proteome Alterations Associated with Neuropsychiatric Symptoms in Cognitive Decline and Alzheimer’s Disease
by
Magdalena Mroczek
,
Christopher Clark
,
Loïc Dayon
,
Gene L. Bowman
and
Julius Popp
Cells 2022, 11(6), 1030; https://doi.org/10.3390/cells11061030 - 18 Mar 2022
Cited by 7 | Viewed by 2007
Abstract
Although neuropsychiatric symptoms (NPS) are common and severely affect older people with cognitive decline, little is known about their underlying molecular mechanisms and relationships with Alzheimer’s disease (AD). The aim of this study was to identify and characterize cerebrospinal fluid (CSF) proteome alterations [...] Read more.
Although neuropsychiatric symptoms (NPS) are common and severely affect older people with cognitive decline, little is known about their underlying molecular mechanisms and relationships with Alzheimer’s disease (AD). The aim of this study was to identify and characterize cerebrospinal fluid (CSF) proteome alterations related to NPS. In a longitudinally followed-up cohort of subjects with normal cognition and patients with cognitive impairment (MCI and mild dementia) from a memory clinic setting, we quantified a panel of 790 proteins in CSF using an untargeted shotgun proteomic workflow. Regression models and pathway enrichment analysis were used to investigate protein alterations related to NPS, and to explore relationships with AD pathology and cognitive decline at follow-up visits. Regression analysis selected 27 CSF proteins associated with NPS. These associations were independent of the presence of cerebral AD pathology (defined as CSF p-tau181/Aβ1–42 > 0.0779, center cutoff). Gene ontology enrichment showed abundance alterations of proteins related to cell adhesion, immune response, and lipid metabolism, among others, in relation to NPS. Out of the selected proteins, three were associated with accelerated cognitive decline at follow-up visits after controlling for possible confounders. Specific CSF proteome alterations underlying NPS may both represent pathophysiological processes independent from AD and accelerate clinical disease progression. Full article
(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)
►▼ Show Figures

Figure 1

Review

Jump to: Research

22 pages, 799 KiB  
Review
New Insights into Neuroinflammation Involved in Pathogenic Mechanism of Alzheimer’s Disease and Its Potential for Therapeutic Intervention
by
Tiantian Li
,
Li Lu
,
Eloise Pember
,
Xinuo Li
,
Bocheng Zhang
and
Zheying Zhu
Cells 2022, 11(12), 1925; https://doi.org/10.3390/cells11121925 - 14 Jun 2022
Cited by 24 | Viewed by 4106
Abstract
Alzheimer’s disease (AD) is the most common form of dementia, affecting more than 50 million people worldwide with an estimated increase to 139 million people by 2050. The exact pathogenic mechanisms of AD remain elusive, resulting in the fact that the current therapeutics [...] Read more.
Alzheimer’s disease (AD) is the most common form of dementia, affecting more than 50 million people worldwide with an estimated increase to 139 million people by 2050. The exact pathogenic mechanisms of AD remain elusive, resulting in the fact that the current therapeutics solely focus on symptomatic management instead of preventative or curative strategies. The two most widely accepted pathogenic mechanisms of AD include the amyloid and tau hypotheses. However, it is evident that these hypotheses cannot fully explain neuronal degeneration shown in AD. Substantial evidence is growing for the vital role of neuroinflammation in AD pathology. The neuroinflammatory hypothesis provides a new, exciting lead in uncovering the underlying mechanisms contributing to AD. This review aims to highlight new insights into the role of neuroinflammation in the pathogenesis of AD, mainly including the involvement of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), nucleotide-binding oligomerization domain, leucine-rich repeat-containing protein 3 (NLRP3)/caspase-1 axis, triggering receptor expressed on myeloid cells 2 (TREM2) and cGAS-STING as key influencers in augmenting AD development. The inflammasomes related to the pathways of NF-κB, NLRP3, TREM2, and cGAS-STING as biomarkers of the neuroinflammation associated with AD, as well as an overview of novel AD treatments based on these biomarkers as potential drug targets reported in the literature or under clinical trials, are explored. Full article
(This article belongs to the Special Issue Alzheimer's Disease: Molecular Mechanisms and Novel Treatment Strategies)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop