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Life
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Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy
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Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (28 February 2025) | Viewed by 11472

Special Issue Editors

Dr. Ivana Shawkatová

E-Mail Website
Guest Editor
Institute of Immunology, Faculty of Medicine, Comenius University in Bratislava, Odborárske nám. 14, 81108 Bratislava, Slovakia
Interests: Alzheimer's disease; immunogenetics; HLA typing; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Juraj Javor

E-Mail Website
Guest Editor
Institute of Immunology, Faculty of Medicine, Comenius University in Bratislava, Odborárske nám. 14, 81108 Bratislava, Slovakia
Interests: Alzheimer's disease; autoimmunity; immunogenetics; neurodegenerative diseases; neuroinflammation; multiple sclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is the most common neurodegenerative disorder in elderly individuals, characterized by a complex pathogenic and clinical profile involving neuronal dysfunction, progressive brain atrophy, and cognitive decline. As the leading cause of dementia worldwide, with approximately 50 million cases, AD poses a substantial medical and socio-economic burden. Despite significant advancements in recent decades, the processes leading to AD-related pathology remain poorly understood. Ongoing efforts to unravel the key cellular and molecular players involved in the development of amyloid and tau pathology, neuroinflammation, neurodegeneration, and other abnormalities offer promising prospects for the identification of new screening and diagnostic biomarkers, as well as the development of novel therapeutic strategies.

In this Special Issue, we aim to publish review and original research articles on the etiology, pathogenesis, diagnostics, and therapy of AD. We invite submissions addressing a broad range of topics including, but not limited to, the following aspects of AD:

  • Genetic, epigenetic, environmental, and lifestyle risk factors for AD.
  • The role of the immune system, oxidative stress, mitochondrial dysfunction, and endocrine, metabolic, and other alterations in the development of AD.
  • The potential link between the gut microbiome and AD.
  • Novel biomarkers for AD diagnostics.
  • Emerging therapeutic approaches.

We welcome contributions that shed light on these areas and advance our understanding of Alzheimer’s disease.

Dr. Ivana Shawkatová
Dr. Juraj Javor
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. Life 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

  • Alzheimer’s disease
  • biomarkers
  • epigenetics
  • genetics
  • genomics
  • immune mediators
  • neurodegeneration
  • neuroinflammation
  • proteomics
  • risk factors
  • therapy
  • transcriptomics

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (6 papers)

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Editorial

Jump to: Research, Review

4 pages, 168 KiB  
Editorial
Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy
by Ivana Shawkatova and Juraj Javor
Life 2025, 15(4), 549; https://doi.org/10.3390/life15040549 - 27 Mar 2025
Viewed by 603
Abstract
As the leading cause of dementia, Alzheimer’s disease (AD) remains one of the most pressing global health challenges, affecting millions worldwide and placing an immense burden on healthcare systems and caregivers [...] Full article
(This article belongs to the Special Issue Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy)

Research

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19 pages, 3870 KiB  
Article
Enhancing Amyloid PET Quantification: MRI-Guided Super-Resolution Using Latent Diffusion Models
by Jay Shah, Yiming Che, Javad Sohankar, Ji Luo, Baoxin Li, Yi Su, Teresa Wu and for the Alzheimer’s Disease Neuroimaging Initiative
Life 2024, 14(12), 1580; https://doi.org/10.3390/life14121580 - 1 Dec 2024
Viewed by 1512
Abstract
Amyloid PET imaging plays a crucial role in the diagnosis and research of Alzheimer’s disease (AD), allowing non-invasive detection of amyloid-β plaques in the brain. However, the low spatial resolution of PET scans limits the accurate quantification of amyloid deposition due to partial [...] Read more.
Amyloid PET imaging plays a crucial role in the diagnosis and research of Alzheimer’s disease (AD), allowing non-invasive detection of amyloid-β plaques in the brain. However, the low spatial resolution of PET scans limits the accurate quantification of amyloid deposition due to partial volume effects (PVE). In this study, we propose a novel approach to addressing PVE using a latent diffusion model for resolution recovery (LDM-RR) of PET imaging. We leverage a synthetic data generation pipeline to create high-resolution PET digital phantoms for model training. The proposed LDM-RR model incorporates a weighted combination of L1, L2, and MS-SSIM losses at both noise and image scales to enhance MRI-guided reconstruction. We evaluated the model’s performance in improving statistical power for detecting longitudinal changes and enhancing agreement between amyloid PET measurements from different tracers. The results demonstrate that the LDM-RR approach significantly improves PET quantification accuracy, reduces inter-tracer variability, and enhances the detection of subtle changes in amyloid deposition over time. We show that deep learning has the potential to improve PET quantification in AD, effectively contributing to the early detection and monitoring of disease progression. Full article
(This article belongs to the Special Issue Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy)
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12 pages, 2881 KiB  
Article
Nilotinib as a Prospective Treatment for Alzheimer’s Disease: Effect on Proteins Involved in Neurodegeneration and Neuronal Homeostasis
by Ankita Srivastava, Heather A. Renna, Maryann Johnson, Katie Sheehan, Saba Ahmed, Thomas Palaia, Aaron Pinkhasov, Irving H. Gomolin, Thomas Wisniewski, Joshua De Leon and Allison B. Reiss
Life 2024, 14(10), 1241; https://doi.org/10.3390/life14101241 - 28 Sep 2024
Viewed by 2465
Abstract
Nilotinib, a tyrosine kinase inhibitor that targets the Abelson tyrosine kinase (c-Abl) signaling pathway, is FDA-approved to treat chronic myeloid leukemia. Nilotinib has properties indicative of a possible utility in neuroprotection that have prompted exploration of repurposing the drug for the treatment of [...] Read more.
Nilotinib, a tyrosine kinase inhibitor that targets the Abelson tyrosine kinase (c-Abl) signaling pathway, is FDA-approved to treat chronic myeloid leukemia. Nilotinib has properties indicative of a possible utility in neuroprotection that have prompted exploration of repurposing the drug for the treatment of Alzheimer’s disease (AD) and Parkinson’s disease (PD). AD is a progressive age-related neurodegenerative disorder characterized by the deposition of extracellular amyloid-β plaques and intracellular neurofibrillary tangles. It is incurable and affects approximately 50 million patients worldwide. Nilotinib reduces c-Abl phosphorylation, amyloid-β levels, and dopaminergic neuron degeneration in preclinical AD models. This study explores the effects of nilotinib on amyloid processing and mitochondrial functioning in the SH-SY5Y human neuroblastoma cell line. SH-SY5Y cells were exposed to nilotinib (1, 5, and 10 µM). Real-time PCR and immunoblot analysis were performed to quantify the expression of genes pertaining to amyloid-β processing and neuronal health. Nilotinib did not significantly change APP, BACE1, or ADAM10 mRNA levels. However, BACE1 protein was significantly increased at 1 µM, and ADAM10 was increased at 10 µM nilotinib without affecting APP protein expression. Further, nilotinib treatment did not affect the expression of genes associated with neuronal health and mitochondrial functioning. Taken together, our findings do not support the efficacy of nilotinib treatment for neuroprotection. Full article
(This article belongs to the Special Issue Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy)
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Review

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27 pages, 856 KiB  
Review
Alzheimer’s Disease and Porphyromonas gingivalis: Exploring the Links
by Ivana Shawkatova, Vladimira Durmanova and Juraj Javor
Life 2025, 15(1), 96; https://doi.org/10.3390/life15010096 - 14 Jan 2025
Cited by 1 | Viewed by 3272
Abstract
Recent research highlights compelling links between oral health, particularly periodontitis, and systemic diseases, including Alzheimer’s disease (AD). Although the biological mechanisms underlying these associations remain unclear, the role of periodontal pathogens, particularly Porphyromonas gingivalis, has garnered significant attention. P. gingivalis, a [...] Read more.
Recent research highlights compelling links between oral health, particularly periodontitis, and systemic diseases, including Alzheimer’s disease (AD). Although the biological mechanisms underlying these associations remain unclear, the role of periodontal pathogens, particularly Porphyromonas gingivalis, has garnered significant attention. P. gingivalis, a major driver of periodontitis, is recognized for its potential systemic effects and its putative role in AD pathogenesis. This review examines evidence connecting P. gingivalis to hallmark AD features, such as amyloid β accumulation, tau hyperphosphorylation, neuroinflammation, and other neuropathological features consistent with AD. Virulence factors, such as gingipains and lipopolysaccharides, were shown to be implicated in blood–brain barrier disruption, neuroinflammation, and neuronal damage. P. gingivalis-derived outer membrane vesicles may serve to disseminate virulence factors to brain tissues. Indirect mechanisms, including systemic inflammation triggered by chronic periodontal infections, are also supposed to exacerbate neurodegenerative processes. While the exact pathways remain uncertain, studies detecting P. gingivalis virulence factors and its other components in AD-affected brains support their possible role in disease pathogenesis. This review underscores the need for further investigation into P. gingivalis-mediated mechanisms and their interplay with host responses. Understanding these interactions could provide critical insights into novel strategies for reducing AD risk through periodontal disease management. Full article
(This article belongs to the Special Issue Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy)
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19 pages, 2143 KiB  
Review
Sexual and Metabolic Differences in Hippocampal Evolution: Alzheimer’s Disease Implications
by José Manuel Martínez-Martos, Vanesa Cantón-Habas, Manuel Rich-Ruíz, María José Reyes-Medina, María Jesús Ramírez-Expósito and María del Pilar Carrera-González
Life 2024, 14(12), 1547; https://doi.org/10.3390/life14121547 - 26 Nov 2024
Cited by 1 | Viewed by 1434
Abstract
Sex differences in brain metabolism and their relationship to neurodegenerative diseases like Alzheimer’s are an important emerging topic in neuroscience. Intrinsic anatomic and metabolic differences related to male and female physiology have been described, underscoring the importance of considering biological sex in studying [...] Read more.
Sex differences in brain metabolism and their relationship to neurodegenerative diseases like Alzheimer’s are an important emerging topic in neuroscience. Intrinsic anatomic and metabolic differences related to male and female physiology have been described, underscoring the importance of considering biological sex in studying brain metabolism and associated pathologies. The hippocampus is a key structure exhibiting sex differences in volume and connectivity. Adult neurogenesis in the dentate gyrus, dendritic spine density, and electrophysiological plasticity contribute to the hippocampus’ remarkable plasticity. Glucose transporters GLUT3 and GLUT4 are expressed in human hippocampal neurons, with proper glucose metabolism being crucial for learning and memory. Sex hormones play a major role, with the aromatase enzyme that generates estradiol increasing in neurons and astrocytes as an endogenous neuroprotective mechanism. Inhibition of aromatase increases gliosis and neurodegeneration after brain injury. Genetic variants of aromatase may confer higher Alzheimer’s risk. Estrogen replacement therapy in postmenopausal women prevents hippocampal hypometabolism and preserves memory. Insulin is also a key regulator of hippocampal glucose metabolism and cognitive processes. Dysregulation of the insulin-sensitive glucose transporter GLUT4 may explain the comorbidity between type II diabetes and Alzheimer’s. GLUT4 colocalizes with the insulin-regulated aminopeptidase IRAP in neuronal vesicles, suggesting an activity-dependent glucose uptake mechanism. Sex differences in brain metabolism are an important factor in understanding neurodegenerative diseases, and future research must elucidate the underlying mechanisms and potential therapeutic implications of these differences. Full article
(This article belongs to the Special Issue Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy)
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14 pages, 229 KiB  
Review
Disease-Specific Risk Models for Predicting Dementia: An Umbrella Review
by Eugene Yee Hing Tang, Jacob Brain, Serena Sabatini, Eduwin Pakpahan, Louise Robinson, Maha Alshahrani, Aliya Naheed, Mario Siervo and Blossom Christa Maree Stephan
Life 2024, 14(11), 1489; https://doi.org/10.3390/life14111489 - 15 Nov 2024
Viewed by 1275
Abstract
Dementia is a leading cause of disability and death globally. Individuals with diseases such as cardiovascular, cardiometabolic and cerebrovascular disease are often at increased dementia risk. However, while numerous models have been developed to predict dementia, they are often not tailored to disease-specific [...] Read more.
Dementia is a leading cause of disability and death globally. Individuals with diseases such as cardiovascular, cardiometabolic and cerebrovascular disease are often at increased dementia risk. However, while numerous models have been developed to predict dementia, they are often not tailored to disease-specific groups. Yet, different disease groups may have unique risk factor profiles and tailored models that account for these differences may have enhanced predictive accuracy. In this review, we synthesise findings from three previous systematic reviews on dementia risk model development and testing to present an overview of the literature on dementia risk prediction modelling in people with a history of disease. Nine studies met the inclusion criteria. Currently, disease-specific models have only been developed in people with a history of diabetes where demographic, disease-specific and comorbidity data were used. Some existing risk models, including CHA2DS2-VASc and CHADS2, have been externally validated for dementia outcomes in those with atrial fibrillation and heart failure. One study developed a dementia risk model for their whole population, which had similar predictive accuracy when applied in a sub-sample with stroke. This emphasises the importance of considering disease status in identifying key predictors for dementia and generating accurate prediction models for dementia. Full article
(This article belongs to the Special Issue Alzheimer’s Disease: Recent Developments in Pathogenesis, Diagnosis, and Therapy)
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