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Alzheimer's Disease: From Pathogenic Mechanisms to Therapy
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Alzheimer's Disease: From Pathogenic Mechanisms to Therapy

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: 15 May 2024 | Viewed by 4644

Special Issue Editors

Dr. Jordi Olloquequi

E-Mail Website
Guest Editor
Department of Biochemistry and Physiology, Physiology Section, School of Pharmacy and Food Sciences, Universitat de Barcelona, 08028 Barcelona, Spain
Interests: pathophysiology; inflammation; cell biology; toxicology; neurodegeneration; COPD
Special Issues, Collections and Topics in MDPI journals
Dr. Miren Ettcheto Arriola

E-Mail Website
Guest Editor
1. Department of Pharmacology, Toxicology and Therapeutic Chemistry, Faculty of Pharmacy and Food Science, University of Barcelona, Barcelona, Spain
2. Biomedical Research Networking Centre in Neurodegenerative Diseases (CIBERNED), Madrid, Spain
3. Institute of Neuroscience, University of Barcelona, Barcelona, Spain
Interests: Alzheimer’s disease; APP/PS1; neuroinflammation; dendritic spines; cognitive impairment; high fat diet; metabolic alterations
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer's disease (AD) is a progressive and debilitating neurodegenerative disorder that affects millions of people worldwide. Despite extensive research efforts, the precise pathogenic mechanisms underlying AD remain unclear, and current treatments provide only symptomatic relief. This Special Issue of the International Journal of Molecular Sciences aims to present the latest advances in our understanding of AD pathogenesis and the development of novel therapeutic strategies.

The scope of the issue covers a broad range of topics related to AD research, including the identification of genetic and epigenetic factors that contribute to disease onset and progression, the elucidation of molecular and cellular mechanisms that underlie AD pathogenesis, and the exploration of new biomarkers for early diagnosis and disease monitoring. Additionally, the issue addresses recent progress in the development of novel therapeutic targets and drug candidates, as well as the assessment of clinical trials and translational studies aimed at bringing promising treatments to the clinic.

We welcome original research articles, reviews, and perspectives that cover these topics, as well as others that shed light on the complex nature of AD and its potential treatments. The Special Issue is intended to be a platform for researchers to share their latest findings and insights, and to stimulate further research in this important field.

Dr. Jordi Olloquequi Gonzalez
Dr. Miren Ettcheto Arriola
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • neurodegeneration
  • pathogenesis
  • biomarkers
  • therapeutics
  • drug development
  • clinical trials
  • translational research
  • genetics
  • epigenetics

Published Papers (3 papers)

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Research

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17 pages, 14378 KiB  
Article
The Protective Effects of Reineckia carnea Ether Fraction against Alzheimer’s Disease Pathology: An Exploration in Caenorhabditis elegans Models
by Hai-Jun Fu, Xing-Yue Zhou, Ya-Ping Li, Xue Chen, Yan-Ni He, Da-Lian Qin, Lu Yu, Chong-Lin Yu, Jian-Ming Wu, An-Guo Wu and Xiao-Gang Zhou
Int. J. Mol. Sci. 2023, 24(22), 16536; https://doi.org/10.3390/ijms242216536 - 20 Nov 2023
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Abstract
Alzheimer’s disease (AD) presents a significant challenge to global healthcare systems, with current treatments offering only modest relief and often bringing unwanted side effects, necessitating the exploration of more effective and safer drugs. In this study, we employed the Caenorhabditis elegans (C. [...] Read more.
Alzheimer’s disease (AD) presents a significant challenge to global healthcare systems, with current treatments offering only modest relief and often bringing unwanted side effects, necessitating the exploration of more effective and safer drugs. In this study, we employed the Caenorhabditis elegans (C. elegans) model, specifically the AD-like CL4176 strain expressing the human Aβ(1–42) protein, to investigate the potential of Reineckia carnea extract and its fractions. Our results showed that the Reineckia carnea ether fraction (REF) notably diminished the paralysis rates of CL4176 worms. Additionally, REF also attenuated the neurotoxicity effects prompted by Tau proteins in the BR5270 worms. Moreover, REF was observed to counteract the accumulation of Aβ and pTau proteins and their induced oxidative stress in C. elegans AD-like models. Mechanistic studies revealed that REF’s benefits were associated with the induction of autophagy in worms; however, these protective effects were nullified when autophagy-related genes were suppressed using RNAi bacteria. Together, these findings highlight Reineckia carnea ether fraction as a promising candidate for AD treatment, warranting further investigation into its autophagy-inducing components and their molecular mechanisms. Full article
(This article belongs to the Special Issue Alzheimer's Disease: From Pathogenic Mechanisms to Therapy)
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15 pages, 2013 KiB  
Article
Identification of Plasma Proteins as Biomarkers for Mild Cognitive Impairment and Alzheimer’s Disease Using Liquid Chromatography–Tandem Mass Spectrometry
by Makoto Inoue, Hideaki Suzuki, Kohji Meno, Shan Liu, Tatsumi Korenaga and Kazuhiko Uchida
Int. J. Mol. Sci. 2023, 24(17), 13064; https://doi.org/10.3390/ijms241713064 - 22 Aug 2023
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Abstract
Blood proteins can be used for biomarkers to monitor the progression of cognitive decline, even in the early stages of disease. In this study, we developed a liquid chromatography–tandem mass spectrometry (LC-MS/MS)-based blood test to identify plasma proteins that can be used to [...] Read more.
Blood proteins can be used for biomarkers to monitor the progression of cognitive decline, even in the early stages of disease. In this study, we developed a liquid chromatography–tandem mass spectrometry (LC-MS/MS)-based blood test to identify plasma proteins that can be used to detect mild cognitive impairment (MCI) and Alzheimer’s disease (AD). Using this system, we quantified plasma proteins using isotope-labeled synthetic peptides. A total of 192 patients, including 63 with AD, 71 with MCI, and 58 non-demented controls (NDCs), were analyzed. Multinomial regression and receiver operating characteristic (ROC) analyses were performed to identify specific combinations of plasma protein panels that could differentiate among NDCs, those with MCI, and those with AD. We identified eight plasma protein biomarker candidates that can be used to distinguish between MCI and AD. These biomarkers were associated with coagulation pathways, innate immunity, lipid metabolism, and nutrition. The clinical potential to differentiate cognitive impairment from NDC was assessed using area under the curve values from ROC analysis, which yielded values of 0.83 for males and 0.71 for females. This LC-MS-based plasma protein panel allows the pathophysiology of AD to be followed through detection of cognitive decline and disease progression markers. Full article
(This article belongs to the Special Issue Alzheimer's Disease: From Pathogenic Mechanisms to Therapy)
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Review

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18 pages, 2325 KiB  
Review
Licochalcone A: A Potential Multitarget Drug for Alzheimer’s Disease Treatment
by Jordi Olloquequi, Miren Ettcheto, Amanda Cano, Ana Fortuna, Joana Bicker, Elena Sánchez-Lopez, Cristian Paz, Jesús Ureña, Ester Verdaguer, Carme Auladell and Antoni Camins
Int. J. Mol. Sci. 2023, 24(18), 14177; https://doi.org/10.3390/ijms241814177 - 16 Sep 2023
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Abstract
Licochalcone A (Lico-A) is a flavonoid compound derived from the root of the Glycyrrhiza species, a plant commonly used in traditional Chinese medicine. While the Glycyrrhiza species has shown promise in treating various diseases such as cancer, obesity, and skin diseases due to [...] Read more.
Licochalcone A (Lico-A) is a flavonoid compound derived from the root of the Glycyrrhiza species, a plant commonly used in traditional Chinese medicine. While the Glycyrrhiza species has shown promise in treating various diseases such as cancer, obesity, and skin diseases due to its active compounds, the investigation of Licochalcone A’s effects on the central nervous system and its potential application in Alzheimer’s disease (AD) treatment have garnered significant interest. Studies have reported the neuroprotective effects of Lico-A, suggesting its potential as a multitarget compound. Lico-A acts as a PTP1B inhibitor, enhancing cognitive activity through the BDNF-TrkB pathway and exhibiting inhibitory effects on microglia activation, which enables mitigation of neuroinflammation. Moreover, Lico-A inhibits c-Jun N-terminal kinase 1, a key enzyme involved in tau phosphorylation, and modulates the brain insulin receptor, which plays a role in cognitive processes. Lico-A also acts as an acetylcholinesterase inhibitor, leading to increased levels of the neurotransmitter acetylcholine (Ach) in the brain. This mechanism enhances cognitive capacity in individuals with AD. Finally, Lico-A has shown the ability to reduce amyloid plaques, a hallmark of AD, and exhibits antioxidant properties by activating the nuclear factor erythroid 2-related factor 2 (Nrf2), a key regulator of antioxidant defense mechanisms. In the present review, we discuss the available findings analyzing the potential of Lico-A as a neuroprotective agent. Continued research on Lico-A holds promise for the development of novel treatments for cognitive disorders and neurodegenerative diseases, including AD. Further investigations into its multitarget action and elucidation of underlying mechanisms will contribute to our understanding of its therapeutic potential. Full article
(This article belongs to the Special Issue Alzheimer's Disease: From Pathogenic Mechanisms to Therapy)
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