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Biomedicines
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Molecular Determinants of Neurodegenerative Diseases
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Molecular Determinants of Neurodegenerative Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 7507

Special Issue Editor

Dr. Carlo Santambrogio

E-Mail Website
Guest Editor
Department of Biotechnology and Biosciences, University of Milano-Bicocca, Milan, Italy
Interests: amyloid aggregation; intrinsically disordered proteins; neurodegenerative disorders; structural proteomics; mass spectrometry; protein-protein protein-ligand interaction; biomarker discovery

Special Issue Information

Dear colleagues,

Protein misfolding and the consequent aggregation and deposition of amyloid plaques are at the basis of severe and diffuse neurodegenerative dysfunctions. The causes of these aberrant processes can be familiar or sporadic, with both genetic and environmental factors triggering the disease. The pathways that lead a functional protein to a pathological state are characterized by a complex network of heterogeneous and transient species, making the investigation of these phenomena extremely challenging. At the same time, a deep knowledge of these molecular processes is necessary in order to fully understand the basis of these pathologies, design innovative drugs, and contrive therapeutic strategies. This Special Issue is focused on scientific contributions highlighting the molecular factors that are critical in the onset or development of the disease (e.g., affecting the protein structure, modulating the aggregation kinetics and the aggregate morphology, inducing or abolishing toxicity, governing the prion-like spreading mechanism, etc.). Examples of such determinants are protein mutations, truncations or post-translational modifications, protein ligands, inhibitors of the aggregation pathway, molecules able to disassemble amyloid fibrils, etc. Original manuscripts, review articles, case reports, and commentaries related to this subject are all welcome.

Dr. Carlo Santambrogio
Guest Editor

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. Biomedicines 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

  • protein misfolding
  • amyloid fibrils
  • aggregation kinetics
  • aggregate morphology
  • protein toxicity
  • prion-like spreading
  • aggregation inhibitor

Published Papers (2 papers)

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Research

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18 pages, 3654 KiB  
Article
Co-Ultramicronized Palmitoylethanolamide/Luteolin Restores Oligodendrocyte Homeostasis via Peroxisome Proliferator-Activated Receptor-α in an In Vitro Model of Alzheimer’s Disease
by Roberta Facchinetti, Marta Valenza, Chiara Gomiero, Giulia Federica Mancini, Luca Steardo, Patrizia Campolongo and Caterina Scuderi
Biomedicines 2022, 10(6), 1236; https://doi.org/10.3390/biomedicines10061236 - 26 May 2022
Cited by 10 | Viewed by 2270
Abstract
Oligodendrocytes are cells fundamental for brain functions as they form the myelin sheath and feed axons. They perform these critical functions thanks to the cooperation with other glial cells, mainly astrocytes. The astrocyte/oligodendrocyte crosstalk needs numerous mediators and receptors, such as peroxisome proliferator-activated [...] Read more.
Oligodendrocytes are cells fundamental for brain functions as they form the myelin sheath and feed axons. They perform these critical functions thanks to the cooperation with other glial cells, mainly astrocytes. The astrocyte/oligodendrocyte crosstalk needs numerous mediators and receptors, such as peroxisome proliferator-activated receptors (PPARs). PPAR agonists promote oligodendrocyte precursor cells (OPCs) maturation in myelinating oligodendrocytes. In the Alzheimer’s disease brain, deposition of beta-amyloid (Aβ) has been linked to several alterations, including astrogliosis and changes in OPCs maturation. However, very little is known about the molecular mechanisms. Here, we investigated for the first time the maturation of OPCs co-cultured with astrocytes in an in vitro model of Aβ1–42 toxicity. We also tested the potential beneficial effect of the anti-inflammatory and neuroprotective composite palmitoylethanolamide and luteolin (co-ultra PEALut), which is known to engage the isoform alfa of the PPARs. Our results show that Aβ1–42 triggers astrocyte reactivity and inflammation and reduces the levels of growth factors important for OPCs maturation. Oligodendrocytes indeed show low cell surface area and few arborizations. Co-ultra PEALut counteracts the Aβ1–42-induced inflammation and astrocyte reactivity preserving the morphology of co-cultured oligodendrocytes through a mechanism that in some cases involves PPAR-α. This is the first evidence of the negative effects exerted by Aβ1–42 on astrocyte/oligodendrocyte crosstalk and discloses a never-explored co-ultra PEALut ability in restoring oligodendrocyte homeostasis. Full article
(This article belongs to the Special Issue Molecular Determinants of Neurodegenerative Diseases)
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Review

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18 pages, 1693 KiB  
Review
The Vascular-Immune Hypothesis of Alzheimer’s Disease
by Rashi I. Mehta and Rupal I. Mehta
Biomedicines 2023, 11(2), 408; https://doi.org/10.3390/biomedicines11020408 - 30 Jan 2023
Cited by 6 | Viewed by 4600
Abstract
Alzheimer’s disease (AD) is a devastating and irreversible neurodegenerative disorder with unknown etiology. While its cause is unclear, a number of theories have been proposed to explain the pathogenesis of AD. In large part, these have centered around potential causes for intracerebral accumulation [...] Read more.
Alzheimer’s disease (AD) is a devastating and irreversible neurodegenerative disorder with unknown etiology. While its cause is unclear, a number of theories have been proposed to explain the pathogenesis of AD. In large part, these have centered around potential causes for intracerebral accumulation of beta-amyloid (βA) and tau aggregates. Yet, persons with AD dementia often exhibit autopsy evidence of mixed brain pathologies including a myriad of vascular changes, vascular brain injuries, complex brain inflammation, and mixed protein inclusions in addition to hallmark neuropathologic lesions of AD, namely insoluble βA plaques and neurofibrillary tangles (NFTs). Epidemiological data demonstrate that overlapping lesions diminish the βA plaque and NFT threshold necessary to precipitate clinical dementia. Moreover, a subset of persons who exhibit AD pathology remain resilient to disease while other persons with clinically-defined AD dementia do not exhibit AD-defining neuropathologic lesions. It is increasingly recognized that AD is a pathologically heterogeneous and biologically multifactorial disease with uncharacterized biologic phenomena involved in its genesis and progression. Here, we review the literature with regard to neuropathologic criteria and incipient AD changes, and discuss converging concepts regarding vascular and immune factors in AD. Full article
(This article belongs to the Special Issue Molecular Determinants of Neurodegenerative Diseases)
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