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Biomedicines
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Alzheimer's Disease—115 Years after Its Discovery 2.0
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Alzheimer's Disease—115 Years after Its Discovery 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 (30 September 2024) | Viewed by 6853

Special Issue Editors

Dr. Susana Cardoso

E-Mail Website
Guest Editor
Center for Neuroscience and Cell Biology, University of Coimbra, 3004-504 Coimbra, Portugal
Interests: diabetes; Alzheimer’s disease; mental disorders; mitochondria; oxidative stress; uncoupling proteins; brain metabolism
Special Issues, Collections and Topics in MDPI journals
Dr. Cristina Carvalho

E-Mail Website
Guest Editor
Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517, Coimbra, Portugal
Interests: Alzheimer’s disease; mitochondrial dysfunction; cell (dys)metabolism; type 2 diabetes
Special Issues, Collections and Topics in MDPI journals
Dr. Sónia Catarina Correia

E-Mail Website
Guest Editor
Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal
Interests: Alzheimer’s disease; mitochondria; brain tolerance; hypoxia
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It has been a long journey since Alois Alzheimer, a dedicated German physician, first linked Auguste Deter’s symptoms of deteriorating memory, disorientation, decreasing speech abilities, and lack of judgment to the detection of two characteristic brain lesions, neurofibrillary tangles, and extracellular deposits that were later named senile plaques—a discovery that would make his name a household term throughout the world! Now, at 115 years after this discovery, the massive international research effort has contributed to uncovering several pieces of key information about the causes and accelerators of the development of Alzheimer’s disease (AD) and its progression. From the amyloid cascade, tau aggregation, inflammation and the immune system, cholinergic hypothesis, vascular alterations, and estrogen alterations to oxidative stress, mitochondrial dysfunction, hypometabolism, insulin resistance, gut dysbiosis, etc., many have been the theories and approaches used to tackle one of science’s most difficult puzzles. And, despite previous failures impeding advancement toward effective treatments, current investigations of new medications, non-pharmacological interventions as well as the development of biomarkers and diagnostic tests to monitor disease presence and progression offer the hope of discovering an opportunity—or window—for preventing or arresting AD progression. In this Commemorative Special Issue, we intend to present an overview of the state-of-the-art of this interesting story including the important recent advances and the latest research and milestones in AD research. For this Special Issue, we welcome the submission of original high-quality research and review articles focused on (i) diagnostic tools; (ii) in vivo and in vitro models of the disease; (iii) molecular mechanisms underlying the onset and progression of the disease; and (iv) therapeutic strategies aimed to counteract the advances of AD.

Dr. Susana Cardoso
Dr. Cristina Carvalho
Dr. Sónia Catarina Correia
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. Biomedicines 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 2600 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

  • diagnostics tools
  • therapeutics
  • Alzheimer’s disease
  • AD hypotheses
  • AD models

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Related Special Issue

Published Papers (4 papers)

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Review

16 pages, 690 KiB  
Review
Disease Modifying Monoclonal Antibodies and Symptomatic Pharmacological Treatment for Alzheimer’s Disease
by Xiaoming Qi, Damir Nizamutdinov, Song Stephen Yi, Erxi Wu and Jason H. Huang
Biomedicines 2024, 12(11), 2636; https://doi.org/10.3390/biomedicines12112636 - 19 Nov 2024
Viewed by 447
Abstract
Alzheimer’s Disease (AD) is an irreversible, progressive syndrome characterized by neurocognitive impairment. Two neuropathological features seen in AD are extracellular amyloid plaques consisting of amyloid beta1-40 and 1-42, and intracellular neurofibrillary tangles (NFTs). For decades, neuroscience research has heavily focused on seeking to [...] Read more.
Alzheimer’s Disease (AD) is an irreversible, progressive syndrome characterized by neurocognitive impairment. Two neuropathological features seen in AD are extracellular amyloid plaques consisting of amyloid beta1-40 and 1-42, and intracellular neurofibrillary tangles (NFTs). For decades, neuroscience research has heavily focused on seeking to understand the primary mechanism of AD and searching for pharmacological approaches for the treatment of dementia. Three monoclonal antibodies that act against amyloid beta—aducanumab, lecanemab, and donanemab—have been approved by the Food and Drug Administration (FDA) for the treatment of mild cognitive impairment and mild AD, in addition to medications for cognitive symptom management such as acetylcholinesterase inhibitors and the N-methyl-D-aspartate (NMDA) antagonist. Further trials should focus on the combination of therapies targeting amyloid plaques and tau pathology. Full article
(This article belongs to the Special Issue Alzheimer's Disease—115 Years after Its Discovery 2.0)
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15 pages, 1213 KiB  
Review
Dendrimers—Novel Therapeutic Approaches for Alzheimer’s Disease
by Magdalena Mroziak, Gracjan Kozłowski, Weronika Kołodziejczyk, Magdalena Pszczołowska, Kamil Walczak, Jan Aleksander Beszłej and Jerzy Leszek
Biomedicines 2024, 12(8), 1899; https://doi.org/10.3390/biomedicines12081899 - 20 Aug 2024
Viewed by 996
Abstract
Dendrimers are covalently bonded globular nanostructures that may be used in the treatment of Alzheimer’s disease (AD). Nowadays, AD therapies are focused on improving cognitive functioning and not causal treatment. However, this may change with the use of dendrimers, which are being investigated [...] Read more.
Dendrimers are covalently bonded globular nanostructures that may be used in the treatment of Alzheimer’s disease (AD). Nowadays, AD therapies are focused on improving cognitive functioning and not causal treatment. However, this may change with the use of dendrimers, which are being investigated as a drug-delivery system or as a drug per se. With their ability to inhibit amyloid formation and their anti-tau properties, they are a promising therapeutic option for AD patients. Studies have shown that dendrimers may inhibit amyloid formation in at least two ways: by blocking fibril growth and by breaking already existing fibrils. Neurofibrillary tangles (NFTs) are abnormal filaments built by tau proteins that can be accumulated in the cell, which leads to the loss of cytoskeletal microtubules and tubulin-associated proteins. Cationic phosphorus dendrimers, with their anti-tau properties, can induce the aggregation of tau into amorphous structures. Drug delivery to mitochondria is difficult due to poor transport across biological barriers, such as the inner mitochondrial membrane, which is highly negatively polarized. Dendrimers may be potential nanocarriers and increase mitochondria targeting. Another considered use of dendrimers in AD treatment is as a drug-delivery system, for example, carbamazepine (CBZ) or tacrine. They can also be used to transport siRNA into neuronal tissue and to carry antioxidants and anti-inflammatory drugs to act protectively on the nervous system. Full article
(This article belongs to the Special Issue Alzheimer's Disease—115 Years after Its Discovery 2.0)
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15 pages, 2937 KiB  
Review
Liposomes against Alzheimer’s Disease: Current Research and Future Prospects
by Christiana Constantinou, Katerina Meliou, Athanasios Skouras, Panoraia Siafaka and Panayiota Christodoulou
Biomedicines 2024, 12(7), 1519; https://doi.org/10.3390/biomedicines12071519 - 8 Jul 2024
Viewed by 1318
Abstract
Alzheimer’s disease, the most common neurodegenerative disease, affects more than 60 million people worldwide, a number that is estimated to double by 2050. Alzheimer’s disease is characterized by progressive memory loss, the impairment of behavior, and mood changes, as well as the disturbed [...] Read more.
Alzheimer’s disease, the most common neurodegenerative disease, affects more than 60 million people worldwide, a number that is estimated to double by 2050. Alzheimer’s disease is characterized by progressive memory loss, the impairment of behavior, and mood changes, as well as the disturbed daily routine of the patient. Although there are some active molecules that can be beneficial by halting the progression of the disease, the blood–brain barrier and other physiological barriers hinder their delivery and, consequently, the appropriate management of the disease. Therefore, drug delivery systems that effectively target and overcome the blood–brain barrier to reach the targeted brain area would improve treatment effectiveness. Liposomes are lipophilic carriers that consist of a phospholipid bilayer structure, simulating the physiological lipidic layer of the blood–brain barrier and enabling better delivery of the drug to the brain. Given that pure liposomes may have less targeting affinity than functionalized liposomes, modification with groups such as lactoferrin, poly(ethylene glycol), and transferrin may improve specificity. In this mini-review, we summarize the literature on the use of liposomes for the treatment of Alzheimer’s disease, focusing on the functionalization moieties of liposomes. In addition, challenges in brain delivery are also discussed. Full article
(This article belongs to the Special Issue Alzheimer's Disease—115 Years after Its Discovery 2.0)
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37 pages, 1157 KiB  
Review
Current Advances in Mitochondrial Targeted Interventions in Alzheimer’s Disease
by Tiago Sousa, Paula I. Moreira and Susana Cardoso
Biomedicines 2023, 11(9), 2331; https://doi.org/10.3390/biomedicines11092331 - 22 Aug 2023
Cited by 6 | Viewed by 3282
Abstract
Alzheimer’s disease is the most prevalent neurodegenerative disorder and affects the lives not only of those who are diagnosed but also of their caregivers. Despite the enormous social, economic and political burden, AD remains a disease without an effective treatment and with several [...] Read more.
Alzheimer’s disease is the most prevalent neurodegenerative disorder and affects the lives not only of those who are diagnosed but also of their caregivers. Despite the enormous social, economic and political burden, AD remains a disease without an effective treatment and with several failed attempts to modify the disease course. The fact that AD clinical diagnosis is most often performed at a stage at which the underlying pathological events are in an advanced and conceivably irremediable state strongly hampers treatment attempts. This raises the awareness of the need to identify and characterize the early brain changes in AD, in order to identify possible novel therapeutic targets to circumvent AD’s cascade of events. One of the most auspicious targets is mitochondria, powerful organelles found in nearly all cells of the body. A vast body of literature has shown that mitochondria from AD patients and model organisms of the disease differ from their non-AD counterparts. In view of this evidence, preserving and/or restoring mitochondria’s health and function can represent the primary means to achieve advances to tackle AD. In this review, we will briefly assess and summarize the previous and latest evidence of mitochondria dysfunction in AD. A particular focus will be given to the recent updates and advances in the strategy options aimed to target faulty mitochondria in AD. Full article
(This article belongs to the Special Issue Alzheimer's Disease—115 Years after Its Discovery 2.0)
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