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Biomolecules
Special Issues
From Biomarkers to Therapy to Puzzle Out Alzheimer’s Disease
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From Biomarkers to Therapy to Puzzle Out Alzheimer’s Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Biomarkers".

Deadline for manuscript submissions: closed (29 February 2024) | Viewed by 52154

Special Issue Editor

Dr. Marta Valenza

E-Mail Website
Guest Editor
Department of Physiology and Pharmacology “Vittorio Erspamer”, SAPIENZA University of Rome—P.le A. Moro, 5, 00185 Rome, Italy
Interests: astrocytes; beta amyloid; luteolin; microglia; neuroinflammation; neuroprotection; palmitoylethanolamide; preclinical Alzheimer’s disease; prodromal Alzheimer’s disease; reactive gliosis; Alzheimer’s disease; astrogliosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We all know that Alzheimer's disease (AD) begins decades before its clinical manifestations. Therefore, ideally, therapy must start very early to be effective. In particular, it must begin before neuronal degeneration and brain atrophy occur, these being irreversible. Thus, there are two puzzles to solve: first, how to be sure that the person actually develops AD over time, and second, what to administer. To date, none of the AD biomarkers are as sensitive as direct examination of tissue at autopsy. Even if AD is accurately diagnosed at the prodromal stage, there are no therapeutics that could be administered. In addition, people with prodromal-stage AD and who are asymptomatic may refuse invasive therapies or medications whose side effects alter or interfere with normal daily life. If new effective drugs for prodromal stage were ever identified and approved, they would be used for decades, making patient adherence to therapy a critical issue. To avoid the risk of increasing unmet clinical need, further pharmacological research is required. This must aim to develop new disease-modifying drugs that can be used in immediately to treat cognitively normal at-risk patients.

This Issue is intended to help stimulate scientific discussion on the use of innovative strategies to solve such puzzles. Original articles looking at identifying the very early signs of AD, at understanding disease progression, and at clarifying which biomarkers reliably predict the development of AD are especially welcome. Additionally, we intend for the Issue to publish studies on innovative pharmacological approaches targeting the very early stages of AD. Reviews and opinion articles discussing such topics are encouraged.

Dr. Marta Valenza
Guest Editor

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. Biomolecules 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 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

  • AD biomarker
  • preclinical AD
  • prodromal AD
  • AD therapy

Published Papers (4 papers)

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Research

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14 pages, 3892 KiB  
Article
Low-Dose Chidamide Treatment Displays Sex-Specific Differences in the 3xTg-AD Mouse
by Jessica Dennison, Armando Mendez, Angela Szeto, Ines Lohse, Claes Wahlestedt and Claude-Henry Volmar
Biomolecules 2023, 13(9), 1324; https://doi.org/10.3390/biom13091324 - 29 Aug 2023
Viewed by 1130
Abstract
Epigenetic compounds have become attractive small molecules for targeting the multifaceted aspects of Alzheimer’s disease (AD). Although AD disproportionately affects women, most of the current literature investigating epigenetic compounds for the treatment of AD do not report sex-specific results. This is remarkable because [...] Read more.
Epigenetic compounds have become attractive small molecules for targeting the multifaceted aspects of Alzheimer’s disease (AD). Although AD disproportionately affects women, most of the current literature investigating epigenetic compounds for the treatment of AD do not report sex-specific results. This is remarkable because there is rising evidence that epigenetic compounds intrinsically affect males and females differently. This manuscript explores the sexual dimorphism observed after chronic, low-dose administration of a clinically relevant histone deacetylase inhibitor, chidamide (Tucidinostat), in the 3xTg-AD mouse model. We found that chidamide treatment significantly improves glucose tolerance and increases expression of glucose transporters in the brain of males. We also report a decrease in total tau in chidamide-treated mice. Differentially expressed genes in chidamide-treated mice were much greater in males than females. Genes involved in the neuroinflammatory pathway and amyloid processing pathway were mostly upregulated in chidamide-treated males while downregulated in chidamide-treated females. This work highlights the need for drug discovery projects to consider sex as a biological variable to facilitate translation. Full article
(This article belongs to the Special Issue From Biomarkers to Therapy to Puzzle Out Alzheimer’s Disease)
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Review

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22 pages, 998 KiB  
Review
Neuroinflammation in Alzheimer’s Disease: A Potential Role of Nose-Picking in Pathogen Entry via the Olfactory System?
by Xian Zhou, Paayal Kumar, Deep J. Bhuyan, Slade O. Jensen, Tara L. Roberts and Gerald W. Münch
Biomolecules 2023, 13(11), 1568; https://doi.org/10.3390/biom13111568 - 24 Oct 2023
Cited by 1 | Viewed by 43605
Abstract
Alzheimer’s disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline and memory impairment. Many possible factors might contribute to the development of AD, including amyloid peptide and tau deposition, but more recent evidence suggests that neuroinflammation may also play an—at [...] Read more.
Alzheimer’s disease (AD) is a complex neurodegenerative disorder characterized by progressive cognitive decline and memory impairment. Many possible factors might contribute to the development of AD, including amyloid peptide and tau deposition, but more recent evidence suggests that neuroinflammation may also play an—at least partial—role in its pathogenesis. In recent years, emerging research has explored the possible involvement of external, invading pathogens in starting or accelerating the neuroinflammatory processes in AD. In this narrative review, we advance the hypothesis that neuroinflammation in AD might be partially caused by viral, bacterial, and fungal pathogens entering the brain through the nose and the olfactory system. The olfactory system represents a plausible route for pathogen entry, given its direct anatomical connection to the brain and its involvement in the early stages of AD. We discuss the potential mechanisms through which pathogens may exploit the olfactory pathway to initiate neuroinflammation, one of them being accidental exposure of the olfactory mucosa to hands contaminated with soil and feces when picking one’s nose. Full article
(This article belongs to the Special Issue From Biomarkers to Therapy to Puzzle Out Alzheimer’s Disease)
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13 pages, 458 KiB  
Review
The Potential of Fasting-Mimicking Diet as a Preventive and Curative Strategy for Alzheimer’s Disease
by Virginia Boccardi, Martina Pigliautile, Anna Giulia Guazzarini and Patrizia Mecocci
Biomolecules 2023, 13(7), 1133; https://doi.org/10.3390/biom13071133 - 14 Jul 2023
Cited by 5 | Viewed by 5064
Abstract
This review examines the potential of fasting-mimicking diets (FMDs) in preventing and treating Alzheimer’s disease (AD). FMDs are low-calorie diets that mimic the physiological and metabolic effects of fasting, including the activation of cellular stress response pathways and autophagy. Recent studies have shown [...] Read more.
This review examines the potential of fasting-mimicking diets (FMDs) in preventing and treating Alzheimer’s disease (AD). FMDs are low-calorie diets that mimic the physiological and metabolic effects of fasting, including the activation of cellular stress response pathways and autophagy. Recent studies have shown that FMDs can reduce amyloid-beta accumulation, tau phosphorylation, and inflammation, as well as improve cognitive function in animal models of AD. Human studies have also reported improvements in AD biomarkers, cognitive functions, and subjective well-being measures following FMDs. However, the optimal duration and frequency of FMDs and their long-term safety and efficacy remain to be determined. Despite these uncertainties, FMDs hold promise as a non-pharmacological approach to AD prevention and treatment, and further research in this area is warranted. Full article
(This article belongs to the Special Issue From Biomarkers to Therapy to Puzzle Out Alzheimer’s Disease)
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Other

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9 pages, 472 KiB  
Brief Report
Potential Neuroprotective Effects of Dietary Omega-3 Fatty Acids on Stress in Alzheimer’s Disease
by Kaitlyn B. Hartnett, Bradley J. Ferguson, Patrick M. Hecht, Luke E. Schuster, Joel I. Shenker, David R. Mehr, Kevin L. Fritsche, Martha A. Belury, Douglas W. Scharre, Adam J. Horwitz, Briana M. Kille, Briann E. Sutton, Paul E. Tatum, C. Michael Greenlief and David Q. Beversdorf
Biomolecules 2023, 13(7), 1096; https://doi.org/10.3390/biom13071096 - 8 Jul 2023
Cited by 2 | Viewed by 1796
Abstract
Background: A large number of individual potentially modifiable factors are associated with risk for Alzheimer’s disease (AD). However, less is known about the interactions between the individual factors. Methods: In order to begin to examine the relationship between a pair of factors, we [...] Read more.
Background: A large number of individual potentially modifiable factors are associated with risk for Alzheimer’s disease (AD). However, less is known about the interactions between the individual factors. Methods: In order to begin to examine the relationship between a pair of factors, we performed a pilot study, surveying patients with AD and controls for stress exposure and dietary omega-3 fatty acid intake to explore their relationship for risk of AD. Results: For individuals with the greatest stress exposure, omega-3 fatty acid intake was significantly greater in healthy controls than in AD patients. There was no difference among those with low stress exposure. Conclusions: These initial results begin to suggest that omega-3 fatty acids may mitigate AD risk in the setting of greater stress exposure. This will need to be examined with larger populations and other pairs of risk factors to better understand these important relationships. Examining how individual risk factors interact will ultimately be important for learning how to optimally decrease the risk of AD. Full article
(This article belongs to the Special Issue From Biomarkers to Therapy to Puzzle Out Alzheimer’s Disease)
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