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Amyloid-β: Structure, Function, and Pathophysiological Significance in Neurodegenerative Diseases 3.0

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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: 20 June 2024 | Viewed by 2176

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Special Issue Editors

Prof. Dr. Masashi Tanaka

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Guest Editor

Department of Physical Therapy, Health Science University, 7187 Kodachi, Fujikawaguchiko-machi, Minamitsuru-gun, Yamanashi 401-0380, Japan
Interests: amyloid-beta; dementia; type 2 diabetes; innate immune system; inflammation; microglia; obesity
Special Issues, Collections and Topics in MDPI journals

Prof. Dr. Kenjiro Ono

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Department of Neurology, Kanazawa University Graduate School of Medical Sciences, 13-1 Takara-machi, Kanazawa 920-8640, Japan
Interests: neurology; dementia; Alzheimer’s disease; Lewy body diseases; amyloid, oligomer; protein aggregation
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Dr. Satoshi Saito

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Guest Editor

Department of Neurology, National Cerebral and Cardiovascular Center, 6-1 Kishibe-Shimmachi, Osaka 564-8565, Japan
Interests: Alzheimer's disease; cerebral amyloid angiopathy; small vessel disease; treatment; translational research
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue “Amyloid-β: Structure, Function, and Pathophysiological Significance in Neurodegenerative Diseases” and Special Issue “Amyloid-β: Structure, Function, and Pathophysiological Significance in Neurodegenerative Diseases 2.0”.

The prevalence of dementia is increasing exponentially worldwide; therefore, its predictive markers and effective treatments should be urgently developed. Considerable studies have revealed the pathological roles of amyloid-β (Aβ) in the development and progression of dementia, namely: Aβ aggregates fibril formation, accumulates senile plaques and blood vessels in the brain, and exhibits cytotoxic effects on neurons and cerebrovascular endothelial cells. These conditions lead to neuronal and vascular injury, thereby resulting in neurodegenerative diseases, such as Alzheimer’s disease (AD) and cerebral amyloid angiopathy, as major causes of dementia. These findings highlight the significance of Aβ as a therapeutic target for dementia, although a new drug focusing on Aβ for the treatment of AD has not yet been developed over the past 15 years. Conversely, recent advances in basic and clinical studies on Aβ and neurodegenerative diseases further reinforce the importance of targeting Aβ and identify the potential novel therapeutic strategies for Aβ-related cognitive impairment.

Here, IJMS sets up this Special Issue focusing on the current understanding and future research directions regarding the structure, function, and pathological significance of Aβ in neurodegenerative diseases. We warmly welcome original manuscripts, review articles, case reports, and commentaries relating to this hot topic.

Prof. Dr. Masashi Tanaka
Prof. Dr. Kenjiro Ono
Dr. Satoshi Saito
Guest Editors

Manuscript Submission Information

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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.

Keywords

Alzheimer’s disease
amyloid-β
cerebral amyloid angiopathy
fibril formation
microglia
neurodegeneration
predictive markers
treatment

Published Papers (2 papers)

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Research

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9 pages, 2173 KiB

Open AccessCommunication

Diffusion Mediates Molecular Transport through the Perivascular Space in the Brain

by Marie Tanaka, Yoko Hirayoshi, Shinobu Minatani, Itsuki Hasegawa and Yoshiaki Itoh

Int. J. Mol. Sci. 2024, 25(5), 2480; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25052480 - 20 Feb 2024

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Abstract

The perivascular space has been proposed as a clearance pathway for degradation products in the brain, including amyloid β, the accumulation of which may induce Alzheimer’s disease. Live images were acquired using a two-photon microscope through a closed cranial window in mice. In topical application experiments, the dynamics of FITC-dextran were evaluated from 30 to 150 min after the application and closure of the window. In continuous injection experiments, image acquisition began before the continuous injection of FITC-dextran. The transport of dextran molecules of different sizes was evaluated. In topical application experiments, circumferential accumulation around the penetrating arteries, veins, and capillaries was observed, even at the beginning of the observation period. No further increases were detected. In continuous injection experiments, a time-dependent increase in the fluorescence intensity was observed around the penetrating arteries and veins. Lower-molecular-weight dextran was transported more rapidly than higher-molecular-weight dextran, especially around the arteries. The largest dextran molecules were not transported significantly during the observation period. The size-dependent transport of dextran observed in the present study strongly suggests that diffusion is the main mechanism mediating substance transport in the perivascular space. Full article

(This article belongs to the Special Issue Amyloid-β: Structure, Function, and Pathophysiological Significance in Neurodegenerative Diseases 3.0)

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Review

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18 pages, 2742 KiB

Open AccessReview

Biological Diagnosis of Alzheimer’s Disease Based on Amyloid Status: An Illustration of Confirmation Bias in Medical Research?

by Benoît Souchet, Alkéos Michaïl, Baptiste Billoir and Jérôme Braudeau

Int. J. Mol. Sci. 2023, 24(24), 17544; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms242417544 - 16 Dec 2023

Cited by 2 | Viewed by 1294

Abstract

Alzheimer’s disease (AD) was first characterized by Dr. Alois Alzheimer in 1906 by studying a demented patient and discovering cerebral amyloid plaques and neurofibrillary tangles. Subsequent research highlighted the roles of Aβ peptides and tau proteins, which are the primary constituents of these lesions, which led to the amyloid cascade hypothesis. Technological advances, such as PET scans using Florbetapir, have made it possible to visualize amyloid plaques in living patients, thus improving AD’s risk assessment. The National Institute on Aging and the Alzheimer’s Association introduced biological diagnostic criteria in 2011, which underlined the amyloid deposits diagnostic value. However, potential confirmation bias may have led researchers to over-rely on amyloid markers independent of AD’s symptoms, despite evidence of their limited specificity. This review provides a critical examination of the current research paradigm in AD, including, in particular, the predominant focus on amyloid and tau species in diagnostics. We discuss the potential multifaceted consequences of this approach and propose strategies to mitigate its overemphasis in the development of new biomarkers. Furthermore, our study presents comprehensive guidelines aimed at enhancing the creation of biomarkers for accurately predicting AD dementia onset. These innovations are crucial for refining patient selection processes in clinical trial enrollment and for the optimization of therapeutic strategies. Overcoming confirmation bias is essential to advance the diagnosis and treatment of AD and to move towards precision medicine by incorporating a more nuanced understanding of amyloid biomarkers. Full article

(This article belongs to the Special Issue Amyloid-β: Structure, Function, and Pathophysiological Significance in Neurodegenerative Diseases 3.0)

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