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Biomedicines
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Molecular Research of Alzheimer's Disease 2.0
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Molecular Research of Alzheimer's Disease 2.0

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 8029

Special Issue Editor

Dr. Lorenzo Falsetti

E-Mail Website
Guest Editor
Department of Emergency Medicine, Internal and Sub-Intensive Medicine, Azienda Ospedaliero-Universitaria "Ospedali Riuniti", 60166 Ancona, Italy
Interests: Alzheimer's disease; neurodegeneration; vascular disease; acute care; critically ill patient
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer’s disease represents a growing health concern, since aging demographics are actively contributing to a significant increase in its prevalence and incidence. The classical neuropathogenetic model, based on brain amyloid plaque deposition, neurofibrillary tangles, and cholinergic system dysfunction, is undergoing reconsideration and integration in light of the failure of both amyloid-targeted and cholinesterase-inhibiting therapies. A better understanding of the relationships between classical pathogenetic pathways and newer hypotheses is urgently required to guide future research and develop effective drugs. The role of risk factors and comorbidities, such as vascular diseases and diabetes mellitus, as well as neurovascular unit dysfunction, is suggesting the existence of newer molecular mechanisms that could represent potential targets for effective Alzheimer’s disease treatments. The aim of this Special Issue of Biomedicines is to provide an overview of the pathophysiologic role of newer and older molecular mechanisms of Alzheimer’s disease and to advance new insights for the development of new therapeutic approaches. Moreover, it will focus on newer candidate markers of disease onset and progression. Both original articles and reviews will be considered for publication in this Special Issue.

Dr. Lorenzo Falsetti
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.

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Related Special Issue

Published Papers (2 papers)

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Research

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11 pages, 1183 KiB  
Article
A Novel Automated Chemiluminescence Method for Detecting Cerebrospinal Fluid Amyloid-Beta 1-42 and 1-40, Total Tau and Phosphorylated-Tau: Implications for Improving Diagnostic Performance in Alzheimer’s Disease
by Marina Arcaro, Chiara Fenoglio, Maria Serpente, Andrea Arighi, Giorgio G. Fumagalli, Luca Sacchi, Stefano Floro, Marianna D’Anca, Federica Sorrentino, Caterina Visconte, Alberto Perego, Elio Scarpini and Daniela Galimberti
Biomedicines 2022, 10(10), 2667; https://doi.org/10.3390/biomedicines10102667 - 21 Oct 2022
Cited by 11 | Viewed by 3213
Abstract
Recently, a fully automated instrument for the detection of the Cerebrospinal Fluid (CSF) biomarker for Alzheimer’s disease (AD) (low concentration of Amyloid-beta 42 (Aβ42), high concentration of total tau (T-tau) and Phosphorylated-tau (P-tau181)), has been implemented, namely CLEIA. We conducted a comparative analysis [...] Read more.
Recently, a fully automated instrument for the detection of the Cerebrospinal Fluid (CSF) biomarker for Alzheimer’s disease (AD) (low concentration of Amyloid-beta 42 (Aβ42), high concentration of total tau (T-tau) and Phosphorylated-tau (P-tau181)), has been implemented, namely CLEIA. We conducted a comparative analysis between ELISA and CLEIA methods in order to evaluate the analytical precision and the diagnostic performance of the novel CLEIA system on 111 CSF samples. Results confirmed a robust correlation between ELISA and CLEIA methods, with an improvement of the accuracy with the new CLEIA methodology in the detection of the single biomarkers and in their ratio values. For Aβ42 regression analysis with Passing–Bablok showed a Pearson correlation coefficient r = 0.867 (0.8120; 0.907% 95% CI p < 0.0001), T-tau analysis: r = 0.968 (0.954; 0.978% 95% CI p < 0.0001) and P-tau181: r = 0.946 (0.922; 0.962 5% 95% CI p < 0.0001). The overall ROC AUC comparison between ROC in ELISA and ROC in CLEIA confirmed a more accurate ROC AUC with the new automatic method: T-tau AUC ELISA = 0.94 (95% CI 0.89; 0.99 p < 0.0001) vs. AUC CLEIA = 0.95 (95% CI 0.89; 1.00 p < 0.0001), and P-tau181 AUC ELISA = 0.91 (95% CI 0.85; 0.98 p < 0.0001) vs. AUC CLEIA = 0.98 (95% CI 0.95; 1.00 p < 0.0001). The performance of the new CLEIA method in automation is comparable and, for tau and P-tau181, even better, as compared with standard ELISA. Hopefully, in the future, automation could be useful in clinical diagnosis and also in the context of clinical studies. Full article
(This article belongs to the Special Issue Molecular Research of Alzheimer's Disease 2.0)
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Review

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24 pages, 1097 KiB  
Review
Homocysteine, Cognitive Functions, and Degenerative Dementias: State of the Art
by Simona Luzzi, Veronica Cherubini, Lorenzo Falsetti, Giovanna Viticchi, Mauro Silvestrini and Alessio Toraldo
Biomedicines 2022, 10(11), 2741; https://doi.org/10.3390/biomedicines10112741 - 28 Oct 2022
Cited by 24 | Viewed by 4016
Abstract
There is strong evidence that homocysteine is a risk factor not only for cerebrovascular diseases but also for degenerative dementias. A recent consensus statement renewed the importance and the role of high levels of homocysteine in cognitive decline in several forms of degenerative [...] Read more.
There is strong evidence that homocysteine is a risk factor not only for cerebrovascular diseases but also for degenerative dementias. A recent consensus statement renewed the importance and the role of high levels of homocysteine in cognitive decline in several forms of degenerative dementia, such as Alzheimer’s disease. Although the molecular mechanisms by which homocysteine causes cell dysfunction are known, both the impact of homocysteine on specific cognitive functions and the relationship between homocysteine level and non-Alzheimer dementias have been poorly investigated. Most of the studies addressing the impact of hyperhomocysteinemia on dementias have not examined the profile of performance across different cognitive domains, and have only relied on screening tests, which provide a very general and coarse-grained picture of the cognitive status of the patients. Yet, trying to understand whether hyperhomocysteinemia is associated with the impairment of specific cognitive functions would be crucial, as it would be, in parallel, learning whether some brain circuits are particularly susceptible to the damage caused by hyperhomocysteinemia. These steps would allow one to (i) understand the actual role of homocysteine in the pathogenesis of cognitive decline and (ii) improve the diagnostic accuracy, differential diagnosis and prognostic implications. This review is aimed at exploring and revising the state of the art of these two strictly related domains. Suggestions for future research are provided. Full article
(This article belongs to the Special Issue Molecular Research of Alzheimer's Disease 2.0)
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