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Focus on Cellular Parkinson’s Disease—from Gut to Brain
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Focus on Cellular Parkinson’s Disease—from Gut to Brain

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (20 July 2022) | Viewed by 20551

Special Issue Editor

Dr. Andrea Bugarcic

E-Mail Website
Guest Editor
National Centre for Naturopathic Medicine, Southern Cross University, 2480 East Lismore, Australia
Interests: cell biology; Parkinson’s disease; neurodegenerative diseases; molecular biology; cell models; herbal medicine; protein biochemistry

Special Issue Information

Dear Colleagues,

Parkinson's disease (PD) is an irreversible neurodegenerative disorder that clinically manifests in uncontrolled motor and specific non-motor symptoms (e.g., constipation). There are two primary cellular hallmark features of Parkinson's disease: an irreversible loss of dopaminergic neurons of the substantia nigra pars compacta located within the midbrain, and the formation of intracellular insoluble aggregates called Lewy bodies (LBs). LBs are deposits of lipids and proteins with a dominant component of the LBs identified as a small protein called alpha-synuclein. There is increasing evidence suggesting an interplay between the aggregation of this protein and dopaminergic cell death. Many cellular models of Parkinson’s disease are used in pre-clinical research, but while laboratory studies provide important mechanistic and drug-development knowledge, they also need to be applicable to clinical practice and translational in nature. This Special Issue of Cells is seeking the submission of papers that use cellular models of PD in the context of mechanistic or drug discovery research while taking the multifactorial clinical manifestation of PD into account. Submissions of primary research using mono- or co-culture in vitro and in vivo systems (including studies on microbiome) for mechanistic studies involving complementary medicines (e.g., herbal medicines or nutritional supplementation) are especially welcome in this Special Issue of Cells, but reviews in the area of cellular Parkinson’s disease with a specific focus on mechanisms of disease and potential novel drugs will also be considered.

Dr. Andrea Bugarcic
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. Cells is an international peer-reviewed open access semimonthly 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

  • Parkinson’s disease
  • cellular model
  • complementary medicine
  • alpha-synuclein
  • neurodegeneration

Published Papers (3 papers)

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Research

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13 pages, 2472 KiB  
Communication
Cellular Therapy Using Epitope-Imprinted Composite Nanoparticles to Remove α-Synuclein from an In Vitro Model
by Mei-Hwa Lee, Jeng-Shiung Jan, James L. Thomas, Yuan-Pin Shih, Jin-An Li, Chien-Yu Lin, Tooru Ooya, Lilla Barna, Mária Mészáros, András Harazin, Gergő Porkoláb, Szilvia Veszelka, Maria A. Deli and Hung-Yin Lin
Cells 2022, 11(16), 2584; https://doi.org/10.3390/cells11162584 - 19 Aug 2022
Cited by 4 | Viewed by 1961
Abstract
Several degenerative disorders of the central nervous system, including Parkinson’s disease (PD), are related to the pathological aggregation of proteins. Antibodies against toxic disease proteins, such as α-synuclein (SNCA), are therefore being developed as possible therapeutics. In this work, one peptide (YVGSKTKEGVVHGVA) from [...] Read more.
Several degenerative disorders of the central nervous system, including Parkinson’s disease (PD), are related to the pathological aggregation of proteins. Antibodies against toxic disease proteins, such as α-synuclein (SNCA), are therefore being developed as possible therapeutics. In this work, one peptide (YVGSKTKEGVVHGVA) from SNCA was used as the epitope to construct magnetic molecularly imprinted composite nanoparticles (MMIPs). These composite nanoparticles were characterized by dynamic light scattering (DLS), high-performance liquid chromatography (HPLC), isothermal titration calorimetry (ITC), Brunauer–Emmett–Teller (BET) analysis, and superconducting quantum interference device (SQUID) analysis. Finally, the viability of brain endothelial cells that were treated with MMIPs was measured, and the extraction of SNCA from CRISPR/dCas9a-activated HEK293T cells from the in vitro model system was demonstrated for the therapeutic application of MMIPs. Full article
(This article belongs to the Special Issue Focus on Cellular Parkinson’s Disease—from Gut to Brain)
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Review

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31 pages, 2447 KiB  
Review
Alpha-Synuclein Aggregation Pathway in Parkinson’s Disease: Current Status and Novel Therapeutic Approaches
by Marija Vidović and Milena G. Rikalovic
Cells 2022, 11(11), 1732; https://doi.org/10.3390/cells11111732 - 24 May 2022
Cited by 36 | Viewed by 10385
Abstract
Following Alzheimer’s, Parkinson’s disease (PD) is the second-most common neurodegenerative disorder, sharing an unclear pathophysiology, a multifactorial profile, and massive social costs worldwide. Despite this, no disease-modifying therapy is available. PD is tightly associated with α-synuclein (α-Syn) deposits, which become organised into insoluble, [...] Read more.
Following Alzheimer’s, Parkinson’s disease (PD) is the second-most common neurodegenerative disorder, sharing an unclear pathophysiology, a multifactorial profile, and massive social costs worldwide. Despite this, no disease-modifying therapy is available. PD is tightly associated with α-synuclein (α-Syn) deposits, which become organised into insoluble, amyloid fibrils. As a typical intrinsically disordered protein, α-Syn adopts a monomeric, random coil conformation in an aqueous solution, while its interaction with lipid membranes drives the transition of the molecule part into an α-helical structure. The central unstructured region of α-Syn is involved in fibril formation by converting to well-defined, β-sheet rich secondary structures. Presently, most therapeutic strategies against PD are focused on designing small molecules, peptides, and peptidomimetics that can directly target α-Syn and its aggregation pathway. Other approaches include gene silencing, cell transplantation, stimulation of intracellular clearance with autophagy promoters, and degradation pathways based on immunotherapy of amyloid fibrils. In the present review, we sum marise the current advances related to α-Syn aggregation/neurotoxicity. These findings present a valuable arsenal for the further development of efficient, nontoxic, and non-invasive therapeutic protocols for disease-modifying therapy that tackles disease onset and progression in the future. Full article
(This article belongs to the Special Issue Focus on Cellular Parkinson’s Disease—from Gut to Brain)
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12 pages, 876 KiB  
Review
Hydrogen Sulfide Produced by Gut Bacteria May Induce Parkinson’s Disease
by Kari Erik Murros
Cells 2022, 11(6), 978; https://doi.org/10.3390/cells11060978 - 12 Mar 2022
Cited by 29 | Viewed by 7536
Abstract
Several bacterial species can generate hydrogen sulfide (H2S). Study evidence favors the view that the microbiome of the colon harbors increased amounts of H2S producing bacteria in Parkinson’s disease. Additionally, H2S can easily penetrate cell membranes and [...] Read more.
Several bacterial species can generate hydrogen sulfide (H2S). Study evidence favors the view that the microbiome of the colon harbors increased amounts of H2S producing bacteria in Parkinson’s disease. Additionally, H2S can easily penetrate cell membranes and enter the cell interior. In the cells, excessive amounts of H2S can potentially release cytochrome c protein from the mitochondria, increase the iron content of the cytosolic iron pool, and increase the amount of reactive oxygen species. These events can lead to the formation of alpha-synuclein oligomers and fibrils in cells containing the alpha-synuclein protein. In addition, bacterially produced H2S can interfere with the body urate metabolism and affect the blood erythrocytes and lymphocytes. Gut bacteria responsible for increased H2S production, especially the mucus-associated species of the bacterial genera belonging to the Desulfovibrionaceae and Enterobacteriaceae families, are likely play a role in the pathogenesis of Parkinson’s disease. Special attention should be devoted to changes not only in the colonic but also in the duodenal microbiome composition with regard to the pathogenesis of Parkinson’s disease. Influenza infections may increase the risk of Parkinson’s disease by causing the overgrowth of H2S-producing bacteria both in the colon and duodenum. Full article
(This article belongs to the Special Issue Focus on Cellular Parkinson’s Disease—from Gut to Brain)
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