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Biomolecules
Special Issues
The Role of Amyloid in Neurological Disorders
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The Role of Amyloid in Neurological Disorders

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Biomacromolecules: Proteins".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 4885

Special Issue Editors

Dr. Marny Fedrigo

E-Mail Website
Guest Editor
Department of Cardiac, Thoracic, Vascular Sciences, and Public Health, University of Padua, 35128 Padua, Italy
Interests: heart and kidney transplantation; antibody mediated rejection; complement and DSA antibody; vasculitis; biomarkers mRNA; miRNA; systemic and cardiac amyloidosis; congenital heart diseases
Special Issues, Collections and Topics in MDPI journals
Dr. Tamara Berno

E-Mail Website
Guest Editor
Hematology Unit, Department of Medicine, Hospital University of Padua, Padova, Italy
Interests: plasma cell dyscrasias in particular multiple myeloma; AL amyloidosis

Special Issue Information

Dear Colleagues,

Interest in extracellular deposits of amorphous protein in the central and peripheral neurological system is growing due to new therapeutic strategies that could improve patients’ survival and quality of life. Amyloid-beta continues to be a most important diagnostic and prognostic issue for Alzheimer's disease (AD) and other neurological disorders. Neuropathy is a common manifestation of both hereditary and acquired forms of systemic amyloidosis and may present with progressive sensorimotor polyneuropathy, focal neuropathy, autonomic neuropathy, and other unusual clinical presentations.

Many aspects have been defined in several papers published; that said, there are many others aspects still to be understood. In particular, we do not yet know how the process of this degenerative disease starts, nor do we understand its mechanisms of progression.

This Special Issue aims to collate expertise on neurological disorders due to amyloid protein; in doing so, it will clarify the role of amyloid in the central and peripheral nervous system and its relationship with the immune system. Novel developments in terms of therapeutic options involving proteins, peptides, and antibodies will also be described.

Dr. Marny Fedrigo
Dr. Tamara Berno
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. Biomolecules 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 2700 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

  • amyloid-beta
  • neurodegenerative disorders
  • aducanumab
  • oligomers
  • cross-amyloid intraction

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Published Papers (4 papers)

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Research

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14 pages, 2836 KiB  
Article
Uptake of 18F-AV45 in the Putamen Provides Additional Insights into Alzheimer’s Disease beyond the Cortex
by Zhengshi Yang, Jefferson W. Kinney, Dietmar Cordes and The Alzheimer’s Disease Neuroimaging Initiative
Biomolecules 2024, 14(2), 157; https://doi.org/10.3390/biom14020157 - 29 Jan 2024
Cited by 1 | Viewed by 1642
Abstract
Cortical uptake in brain amyloid positron emission tomography (PET) is increasingly used for the biological diagnosis of Alzheimer’s disease (AD); however, the clinical and biological relevance of the striatum beyond the cortex in amyloid PET scans remains unclear. A total of 513 amyloid-positive [...] Read more.
Cortical uptake in brain amyloid positron emission tomography (PET) is increasingly used for the biological diagnosis of Alzheimer’s disease (AD); however, the clinical and biological relevance of the striatum beyond the cortex in amyloid PET scans remains unclear. A total of 513 amyloid-positive participants having 18F-AV45 amyloid PET scans available were included in the analysis. The associations between cognitive scores and striatal uptake were analyzed. The participants were categorized into three groups based on the residual from the linear fitting between 18F-AV45 uptake in the putamen and the cortex in the order of HighP > MidP > LowP group. We then examined the differences between these three groups in terms of clinical diagnosis, APOE genotype, CSF phosphorylated tau (ptau) concentration, hippocampal volume, entorhinal thickness, and cognitive decline rate to evaluate the additional insights provided by the putamen beyond the cortex. The 18F-AV45 uptake in the putamen was more strongly associated with ADAS-cog13 and MoCA scores (p < 0.001) compared to the uptake in the caudate nucleus. Despite comparable cortical uptakes, the HighP group had a two-fold higher risk of being ε4-homozygous or diagnosed with AD dementia compared to the LowP group. These three groups had significantly different CSF ptau concentration, hippocampal volume, entorhinal thickness, and cognitive decline rate. These findings suggest that the assessment of 18F-AV45 uptake in the putamen is of unique value for evaluating disease severity and predicting disease progression. Full article
(This article belongs to the Special Issue The Role of Amyloid in Neurological Disorders)
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Review

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15 pages, 577 KiB  
Review
Targeting Protein Aggregation in ALS
by Michele Perni and Benedetta Mannini
Biomolecules 2024, 14(10), 1324; https://doi.org/10.3390/biom14101324 - 18 Oct 2024
Viewed by 1041
Abstract
Proteinopathies involve the abnormal accumulation of specific proteins. Maintaining the balance of the proteome is a finely regulated process managed by a complex network of cellular machinery responsible for protein synthesis, folding, and degradation. However, stress and ageing can disrupt this balance, leading [...] Read more.
Proteinopathies involve the abnormal accumulation of specific proteins. Maintaining the balance of the proteome is a finely regulated process managed by a complex network of cellular machinery responsible for protein synthesis, folding, and degradation. However, stress and ageing can disrupt this balance, leading to widespread protein aggregation. Currently, several therapies targeting protein aggregation are in clinical trials for ALS. These approaches mainly focus on two strategies: addressing proteins that are prone to aggregation due to mutations and targeting the cellular mechanisms that maintain protein homeostasis to prevent aggregation. This review will cover these emerging drugs. Advances in ALS research not only offer hope for better outcomes for ALS patients but also provide valuable insights and methodologies that can benefit the broader field of neurodegenerative disease drug discovery. Full article
(This article belongs to the Special Issue The Role of Amyloid in Neurological Disorders)
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20 pages, 1051 KiB  
Review
Are Women with Polycystic Ovary Syndrome at Increased Risk of Alzheimer Disease? Lessons from Insulin Resistance, Tryptophan and Gonadotropin Disturbances and Their Link with Amyloid-Beta Aggregation
by Joachim Sobczuk, Katarzyna Paczkowska, Szymon Andrusiów, Marek Bolanowski and Jacek Daroszewski
Biomolecules 2024, 14(8), 918; https://doi.org/10.3390/biom14080918 - 28 Jul 2024
Viewed by 1148
Abstract
Alzheimer disease, the leading cause of dementia, and polycystic ovary syndrome, one of the most prevalent female endocrine disorders, appear to be unrelated conditions. However, studies show that both disease entities have common risk factors, and the amount of certain protein marker of [...] Read more.
Alzheimer disease, the leading cause of dementia, and polycystic ovary syndrome, one of the most prevalent female endocrine disorders, appear to be unrelated conditions. However, studies show that both disease entities have common risk factors, and the amount of certain protein marker of neurodegeneration is increased in PCOS. Reports on the pathomechanism of both diseases point to the possibility of common denominators linking them. Dysregulation of the kynurenine pathway, insulin resistance, and impairment of the hypothalamic-pituitary-gonadal axis, which are correlated with amyloid-beta aggregation are these common areas. This article discusses the relationship between Alzheimer disease and polycystic ovary syndrome, with a particular focus on the role of disorders of tryptophan metabolism in both conditions. Based on a review of the available literature, we concluded that systemic changes occurring in PCOS influence the increased risk of neurodegeneration. Full article
(This article belongs to the Special Issue The Role of Amyloid in Neurological Disorders)
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Other

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14 pages, 5781 KiB  
Perspective
Neuroradiological Findings in Cerebral Amyloid Angiopathy with a Particular Consideration of the Boston Criteria 2.0: An Imaging Review
by Ulf Jensen-Kondering, Katharina Heß, Alexander Neumann and Nils G. Margraf
Biomolecules 2024, 14(11), 1459; https://doi.org/10.3390/biom14111459 - 17 Nov 2024
Viewed by 535
Abstract
In the elderly, cerebral amyloid angiopathy (CAA) is the most common cause for intracranial lobar hemorrhages. CAA is caused by the accumulation of amyloid-β fibrils in cortical and leptomeningeal vessels. In 2022, the Boston Criteria 2.0 became the new diagnostic standard for CAA, [...] Read more.
In the elderly, cerebral amyloid angiopathy (CAA) is the most common cause for intracranial lobar hemorrhages. CAA is caused by the accumulation of amyloid-β fibrils in cortical and leptomeningeal vessels. In 2022, the Boston Criteria 2.0 became the new diagnostic standard for CAA, following the Modified Boston Criteria of 2010. The diagnostic criteria are a composite of clinical, imaging and histopathological findings. In the latest version of the Boston Criteria, neuroradiological imaging findings were even expanded compared to the previous version. Crucially, the correct application of the diagnostic criteria is necessary to avoid over- and underdiagnosis. The aim of this review is to demonstrate the diagnostic criteria for CAA with an emphasis on typical imaging findings which are part of the Boston Criteria 2.0 and other imaging findings suggestive of CAA. Full article
(This article belongs to the Special Issue The Role of Amyloid in Neurological Disorders)
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