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Life
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Alzheimer's Disease: From Pathogenesis to Therapy
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Alzheimer's Disease: From Pathogenesis to Therapy

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

Deadline for manuscript submissions: closed (26 January 2024) | Viewed by 6758

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, AD is the leading cause of dementia worldwide, with approximately 50 million cases, and 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 life-style risk factors for AD;
  • The role of the immune system, oxidative stress, mitochondrial dysfunction, 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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Published Papers (3 papers)

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Research

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11 pages, 246 KiB  
Article
Association of Loneliness with Functional and Cognitive Status in Minor and Major Neurocognitive Disorders
by Maria Claudia Moretti, Iris Bonfitto, Luciano Nieddu, Ivana Leccisotti, Savino Dimalta, Giovanni Moniello, Madia Lozupone, Antonello Bellomo, Francesco Panza, Carlo Avolio and Mario Altamura
Life 2024, 14(10), 1216; https://doi.org/10.3390/life14101216 - 24 Sep 2024
Viewed by 1105
Abstract
Background: Neurocognitive disorders (NCDs) have a variable decline in cognitive function, while loneliness was associated with cognitive impairment and increased dementia risk. In the present study, we examined the associations of loneliness with functional and cognitive status in patients with minor (mild cognitive [...] Read more.
Background: Neurocognitive disorders (NCDs) have a variable decline in cognitive function, while loneliness was associated with cognitive impairment and increased dementia risk. In the present study, we examined the associations of loneliness with functional and cognitive status in patients with minor (mild cognitive impairment) and major NCDs (dementia). Methods: We diagnosed mild NCD (n = 42) and major NCD (n = 164) through DSM-5 criteria on 206 participants aged > 65 years using the UCLA 3-Item Loneliness Scale (UCLA-3) to evaluate loneliness, the activities of daily living (ADL) and the instrumental activities of daily living (IADL) scales to measure functional status, and Mini-Mental State Examination (MMSE) to assess cognitive functions. Results: In a multivariate regression model, the effect of loneliness on cognitive functions was negative in major (β = −1.05, p < 0.0001) and minor NCD (β = −0.06, p < 0.01). In the fully adjusted multivariate regression model (sex–age–education–multimorbidity–depressive symptoms–antidementia drug treatment), the effect of loneliness remained negative for major NCD and became positive for minor NCD (β = 0.09, p < 0.001). The effect of loneliness on IADL (β = −0.26, p < 0.0001) and ADL (β = −0.24, p < 0.001) showed a negative effect for major NCD across the different models, while for minor NCD, the effect was positive (IADL: β = 0.26, p < 0.0001; ADL: β = 0.05, p = 0.01). Minor NCD displayed different levels of MMSE (β = 6.68, p < 0.001) but not ADL or IADL, compared to major NCD for the same levels of loneliness. MANOVA pill test suggested a statistically significant and different interactive effect of loneliness on functional and cognitive variables between minor and major NCDs. Conclusions: We confirmed the relationships between loneliness and cognitive and functional status in major NCD, observing a novel trend in minor NCD. Full article
(This article belongs to the Special Issue Alzheimer's Disease: From Pathogenesis to Therapy)
17 pages, 722 KiB  
Article
Adiponectin Gene Polymorphisms: A Case–Control Study on Their Role in Late-Onset Alzheimer’s Disease Risk
by Juraj Javor, Vladimíra Ďurmanová, Kristína Klučková, Zuzana Párnická, Dominika Radošinská, Stanislav Šutovský, Barbora Vašečková, Veronika Režnáková, Mária Králová, Karin Gmitterová, Štefan Zorad and Ivana Shawkatová
Life 2024, 14(3), 346; https://doi.org/10.3390/life14030346 - 7 Mar 2024
Cited by 2 | Viewed by 1418
Abstract
Adiponectin, a hormone secreted by adipose tissue, plays a complex role in regulating metabolic homeostasis and has also garnered attention for its potential involvement in the pathogenesis of late-onset Alzheimer’s disease (LOAD). The objective of this study was to investigate the association of [...] Read more.
Adiponectin, a hormone secreted by adipose tissue, plays a complex role in regulating metabolic homeostasis and has also garnered attention for its potential involvement in the pathogenesis of late-onset Alzheimer’s disease (LOAD). The objective of this study was to investigate the association of ADIPOQ variants with plasma adiponectin levels and LOAD risk in subjects from the Slovak Caucasian population. For this purpose, 385 LOAD patients and 533 controls without cognitive impairment were recruited and genotyped for a total of eighteen ADIPOQ single nucleotide polymorphisms (SNPs). Both single-locus and haplotype-based logistic regression analyses were employed to assess the association of SNPs with LOAD risk, while linear regression analysis was used to explore their influence on adiponectin levels in LOAD patients. ADIPOQ variants rs822395 and rs2036373 in intron 1 were found to significantly elevate total adiponectin levels after accounting for several potential confounders. Additional SNPs in the 5′ region and intron 1 exhibited a non-significant trend of association with adiponectin. However, none of the ADIPOQ SNPs showed an association with LOAD risk, neither in the whole-group analysis nor in subgroup analyses after stratification for sex or the APOE ε4 allele, a well-established LOAD risk factor. In summary, while adiponectin has emerged as a potential contributor to the development of LOAD, this study did not unveil any significant involvement of its gene variants in susceptibility to the disease. Full article
(This article belongs to the Special Issue Alzheimer's Disease: From Pathogenesis to Therapy)
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Review

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27 pages, 888 KiB  
Review
Exercise Intervention for Alzheimer’s Disease: Unraveling Neurobiological Mechanisms and Assessing Effects
by Jianchang Ren and Haili Xiao
Life 2023, 13(12), 2285; https://doi.org/10.3390/life13122285 - 30 Nov 2023
Cited by 4 | Viewed by 3736
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disease and a major cause of age-related dementia, characterized by cognitive dysfunction and memory impairment. The underlying causes include the accumulation of beta-amyloid protein (Aβ) in the brain, abnormal phosphorylation, and aggregation of tau protein within [...] Read more.
Alzheimer’s disease (AD) is a progressive neurodegenerative disease and a major cause of age-related dementia, characterized by cognitive dysfunction and memory impairment. The underlying causes include the accumulation of beta-amyloid protein (Aβ) in the brain, abnormal phosphorylation, and aggregation of tau protein within nerve cells, as well as neuronal damage and death. Currently, there is no cure for AD with drug therapy. Non-pharmacological interventions such as exercise have been widely used to treat AD, but the specific molecular and biological mechanisms are not well understood. In this narrative review, we integrate the biology of AD and summarize the knowledge of the molecular, neural, and physiological mechanisms underlying exercise-induced improvements in AD progression. We discuss various exercise interventions used in AD and show that exercise directly or indirectly affects the brain by regulating crosstalk mechanisms between peripheral organs and the brain, including “bone–brain crosstalk”, “muscle–brain crosstalk”, and “gut–brain crosstalk”. We also summarize the potential role of artificial intelligence and neuroimaging technologies in exercise interventions for AD. We emphasize that moderate-intensity, regular, long-term exercise may improve the progression of Alzheimer’s disease through various molecular and biological pathways, with multimodal exercise providing greater benefits. Through in-depth exploration of the molecular and biological mechanisms and effects of exercise interventions in improving AD progression, this review aims to contribute to the existing knowledge base and provide insights into new therapeutic strategies for managing AD. Full article
(This article belongs to the Special Issue Alzheimer's Disease: From Pathogenesis to Therapy)
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