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Molecular Pathogenesis of Alzheimer's Disease 2.0
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Molecular Pathogenesis of Alzheimer's Disease 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 15314

Special Issue Editors

Dr. Agueda A. Rostagno

E-Mail Website
Guest Editor
NYU, Department of Pathology, Grossman School of Medicine, 550 First Avenue, New York, NY 10016, USA
Interests: Alzheimer's disease; amyloidosis; neurodegenerative disorders, autophagy; apoptosis; mitochondrial dysfunction; oxidative stress; metabolic dysregulation; cerebral amyloid angiopathy; molecular chaperones; immunohistochemistry; neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Jorge Ghiso

E-Mail Website
Guest Editor
Department of Pathology, Grossman School of Medicine, New York University, New York, NY 10016, USA
Interests: Alzheimer disease; neurodegenerative disorders; systemic and cerebral amyloidoses; aging; proteomics; post-translational modifications; blood-brain-barrier; amyloid; neurofibrillary tangles; cerebral amyloid angiopathy; cerebral hemorrhage; translational approaches; mouse models
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to address contemporary knowledge related to the pathogenesis of Alzheimer’s disease (AD), the most common form of age-related progressive neurodegenerative disorder in humans. Because of the growing elderly population worldwide, the WHO estimates that the disease will affect more than 115 million individuals by 2050 with a projected healthcare cost of more than $1 trillion. The familial forms, which represent only a small percentage of the cases, are characterized by mutations in three major genes, the amyloid precursor protein (APP), the presenilin1 (PSEN1), and the presenilin 2 (PSEN2)). In contrast, it is widely accepted that sporadic AD, which exhibits a significantly higher prevalence in individuals>65 years of age and accounts for more than 95% of cases, is multifactorial with a number of different pathogenic pathways identified as crucial contributors to the disease. Overall, genetic complexity, epigenetic control, and metabolic turmoil contribute to the ambiguous view of the disease and make it difficult to identify causal relationships between different possible molecular etiologic factors. While extracellular senile plaques and cerebrovascular amyloid-β deposits together with intracellular neurofibrillary tangles, and loss of synapses are the most prominent neuropathological markers of AD, neuroinflammation, alterations in brain metabolism, changes in mitochondrial bioenergetics, and oxidative stress mechanisms, are now considered key players in the disease. 
This special issue aims to provide insight into the interplay between the complex molecular pathways contributing to metabolic and synaptic alterations, neuroinflammatory mechanisms, vascular dysfunction, and cognitive impairment associated with AD and other neurodegenerative conditions sharing common pathogenic mechanisms. We welcome contributions in all aspects of the disease pathogenesis as well as translational approaches based on nanomedicine, stem cell therapies as well as the use of immunotherapeutic and pharmacologic agents, in the form of original research articles, reviews, perspectives, and commentaries.

Dr. Agueda A. Rostagno
Prof. Dr. Jorge Ghiso
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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.

Published Papers (4 papers)

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Research

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11 pages, 1836 KiB  
Article
Evaluation of Synaptic and Axonal Dysfunction Biomarkers in Alzheimer’s Disease and Mild Cognitive Impairment Based on CSF and Bioinformatic Analysis
by Maciej Dulewicz, Agnieszka Kulczyńska-Przybik, Renata Borawska, Agnieszka Słowik and Barbara Mroczko
Int. J. Mol. Sci. 2022, 23(18), 10867; https://doi.org/10.3390/ijms231810867 - 17 Sep 2022
Cited by 3 | Viewed by 1871
Abstract
Synaptic loss and dysfunction are one of the earliest signs of neurodegeneration associated with cognitive decline in Alzheimer’s disease (AD) and other neurodegenerative diseases. This study aimed to assess the relationships between biological processes of the synaptic pathology underlying AD, molecular functions, and [...] Read more.
Synaptic loss and dysfunction are one of the earliest signs of neurodegeneration associated with cognitive decline in Alzheimer’s disease (AD) and other neurodegenerative diseases. This study aimed to assess the relationships between biological processes of the synaptic pathology underlying AD, molecular functions, and dynamics of the change concentrations of selected proteins reflecting synaptic and axonal pathology in dementia stages. Neurogranin (Ng), neuronal pentraxin receptor (NPTXR), and Visinin-like protein 1 (VILIP1) concentrations were measured in the cerebrospinal fluid (CSF) of MCI, AD, and non-demented controls (CTRL) using quantitative immunological methods. Gene ontology (GO) enrichment analysis was used for the functional analysis of tested proteins. The CSF Aβ42/Ng ratio was significantly different between all the compared groups. The CSF NPTXR/Ng ratio was significantly different between MCI compared to CTRL and AD compared to CTRL. The GO enrichment analysis revealed that two terms (the Biological Process (BP) and Cellular Component (CC) levels) are significantly enriched for NPTXR and Ng but not for VILIP1. Both Ng and NPTXR concentrations in CSF are promising synaptic dysfunction biomarkers for the early diagnosis of the disease. Moreover, both proteins are biochemically associated with classical biomarkers and VILIP-1. Mapping shared molecular and biological functions for the tested proteins by GO enrichment analysis may be beneficial in screening and setting new research targets. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Alzheimer's Disease 2.0)
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Review

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32 pages, 4483 KiB  
Review
Blood–Brain Barrier Breakdown in Alzheimer’s Disease: Mechanisms and Targeted Strategies
by Amer E. Alkhalifa, Nour F. Al-Ghraiybah, Julia Odum, John G. Shunnarah, Nataleigh Austin and Amal Kaddoumi
Int. J. Mol. Sci. 2023, 24(22), 16288; https://doi.org/10.3390/ijms242216288 - 14 Nov 2023
Cited by 4 | Viewed by 3408
Abstract
The blood–brain barrier (BBB) is a unique and selective feature of the central nervous system’s vasculature. BBB dysfunction has been observed as an early sign of Alzheimer’s Disease (AD) before the onset of dementia or neurodegeneration. The intricate relationship between the BBB and [...] Read more.
The blood–brain barrier (BBB) is a unique and selective feature of the central nervous system’s vasculature. BBB dysfunction has been observed as an early sign of Alzheimer’s Disease (AD) before the onset of dementia or neurodegeneration. The intricate relationship between the BBB and the pathogenesis of AD, especially in the context of neurovascular coupling and the overlap of pathophysiology in neurodegenerative and cerebrovascular diseases, underscores the urgency to understand the BBB’s role more deeply. Preserving or restoring the BBB function emerges as a potentially promising strategy for mitigating the progression and severity of AD. Molecular and genetic changes, such as the isoform ε4 of apolipoprotein E (ApoEε4), a significant genetic risk factor and a promoter of the BBB dysfunction, have been shown to mediate the BBB disruption. Additionally, receptors and transporters like the low-density lipoprotein receptor-related protein 1 (LRP1), P-glycoprotein (P-gp), and the receptor for advanced glycation end products (RAGEs) have been implicated in AD’s pathogenesis. In this comprehensive review, we endeavor to shed light on the intricate pathogenic and therapeutic connections between AD and the BBB. We also delve into the latest developments and pioneering strategies targeting the BBB for therapeutic interventions, addressing its potential as a barrier and a carrier. By providing an integrative perspective, we anticipate paving the way for future research and treatments focused on exploiting the BBB’s role in AD pathogenesis and therapy. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Alzheimer's Disease 2.0)
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28 pages, 1237 KiB  
Review
Inflammatory Processes in Alzheimer’s Disease—Pathomechanism, Diagnosis and Treatment: A Review
by Bartosz Twarowski and Mariola Herbet
Int. J. Mol. Sci. 2023, 24(7), 6518; https://doi.org/10.3390/ijms24076518 - 30 Mar 2023
Cited by 15 | Viewed by 5090
Abstract
Alzheimer’s disease is one of the most commonly diagnosed cases of senile dementia in the world. It is an incurable process, most often leading to death. This disease is multifactorial, and one factor of this is inflammation. Numerous mediators secreted by inflammatory cells [...] Read more.
Alzheimer’s disease is one of the most commonly diagnosed cases of senile dementia in the world. It is an incurable process, most often leading to death. This disease is multifactorial, and one factor of this is inflammation. Numerous mediators secreted by inflammatory cells can cause neuronal degeneration. Neuritis may coexist with other mechanisms of Alzheimer’s disease, contributing to disease progression, and may also directly underlie AD. Although much has been established about the inflammatory processes in the pathogenesis of AD, many aspects remain unexplained. The work is devoted in particular to the pathomechanism of inflammation and its role in diagnosis and treatment. An in-depth and detailed understanding of the pathomechanism of neuroinflammation in Alzheimer’s disease may help in the development of diagnostic methods for early diagnosis and may contribute to the development of new therapeutic strategies for the disease. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Alzheimer's Disease 2.0)
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17 pages, 321 KiB  
Review
The Role of Fecal Microbiota Transplantation in the Treatment of Neurodegenerative Diseases: A Review
by Julie-Anne T. Matheson and R. M. Damian Holsinger
Int. J. Mol. Sci. 2023, 24(2), 1001; https://doi.org/10.3390/ijms24021001 - 05 Jan 2023
Cited by 21 | Viewed by 3999
Abstract
Neurodegenerative diseases are highly prevalent but poorly understood, and with few treatment options despite decades of intense research, attention has recently shifted toward other mediators of neurological disease that may present future targets for therapeutic research. One such mediator is the gut microbiome, [...] Read more.
Neurodegenerative diseases are highly prevalent but poorly understood, and with few treatment options despite decades of intense research, attention has recently shifted toward other mediators of neurological disease that may present future targets for therapeutic research. One such mediator is the gut microbiome, which communicates with the brain through the gut–brain axis and has been implicated in various neurological disorders. Alterations in the gut microbiome have been associated with numerous neurological and other diseases, and restoration of the dysbiotic gut has been shown to improve disease conditions. One method of restoring a dysbiotic gut is via fecal microbiota transplantation (FMT), recolonizing the “diseased” gut with normal microbiome. Fecal microbiota transplantation is a treatment method traditionally used for Clostridium difficile infections, but it has recently been used in neurodegenerative disease research as a potential treatment method. This review aims to present a summary of neurodegenerative research that has used FMT, whether as a treatment or to investigate how the microbiome influences pathogenesis. Full article
(This article belongs to the Special Issue Molecular Pathogenesis of Alzheimer's Disease 2.0)
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