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Experimental Diagnostics and Therapeutics in Parkinson’s Disease
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Experimental Diagnostics and Therapeutics in Parkinson’s Disease

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

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 14138

Special Issue Editor

Prof. Dr. Eng King Tan

E-Mail Website
Guest Editor
Department of Neurology, National Neuroscience Institute, 20 College Road, Singapore 169856, Singapore
Interests: Parkinson’s disease essential tremor; neurotranplantations; neuroimaging; regeneration medicine

Special Issue Information

Dear Colleagues,

Parkinson’s disease (PD), a common age-related progressive neurodegenerative disorder, is clinically characterized by tremor, bradykinesia, rigidity, and postural imbalance and various non-motor symptoms such as constipation, cognitive impairment, and neuropsychiatric complaints.

The primary pathology of PD is the loss of dopaminergic neurons in the substantia nigra and cellular loss in other brain regions. Both genetic and environmental factors and aging contribute to the underlying pathogenesis.

The identification of monogenic forms of PD and advancements in technology have facilitated the development of better in vitro and in vivo models that have elucidated several new pathophysiologic clues that have, in turn, unravelled several potential new therapeutic targets.  In addition,

several experimental treatments ranging from symptomatic to disease-modifying therapies have led to clinical drug trials and have created considerable excitement and hope for patients with PD.  In this Special Issue, entitled “Experimental Diagnostics and Therapeutics in

Parkinson’s disease”, we encourage submissions of research that uses experimental models which can provide novel pathophysiologic insights, studies that develop new strategies to facilitate the development of better animal models, new angles, or new ways to study the key molecular hallmarks of

PD (e.g., mitochondrial oxidative phosphorylation, autophagy-lysosomal metabolism, immune dysregulation, etc.), and studies that use different experimental approaches such as gene therapy, immunotherapy, and cell therapy.

Prof. Dr. Eng King Tan
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.

Published Papers (4 papers)

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Research

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13 pages, 2163 KiB  
Article
Elevated Monoamine Oxidase-A in Anterior Cingulate of Post-Mortem Human Parkinson’s Disease: A Potential Surrogate Biomarker for Lewy Bodies?
by Jogeshwar Mukherjee, Reisha M. Ladwa, Christopher Liang and Amina U. Syed
Cells 2022, 11(24), 4000; https://doi.org/10.3390/cells11244000 - 10 Dec 2022
Cited by 6 | Viewed by 1521
Abstract
Lewy bodies (LB) play a neuropathological role in Parkinson’s disease (PD). Our goal was to evaluate LB using anti-ubiquitin immunohistochemistry (UIHC) and find correlations with monoamine oxidase-A (MAO-A) using imaging agent, [18F]FAZIN3. Human post-mortem anterior cingulate (AC) and corpus callosum (CC) [...] Read more.
Lewy bodies (LB) play a neuropathological role in Parkinson’s disease (PD). Our goal was to evaluate LB using anti-ubiquitin immunohistochemistry (UIHC) and find correlations with monoamine oxidase-A (MAO-A) using imaging agent, [18F]FAZIN3. Human post-mortem anterior cingulate (AC) and corpus callosum (CC) from control subjects (CN), n = 6; age 81–90 LB = 0 and PD, n = 6, age 77–89, LB = III–IV were sectioned (10 μm slices). Brain slices were immunostained with anti-ubiquitin for LB (UIHC) and analyzed using QuPath for percent anti-ubiquitin per unit area (μm2). Adjacent brain slices were incubated with [18F]FAZIN3 and cortical layers I–III, IV–VI and CC (white matter) regions were quantified for the binding of [18F]FAZIN3. UIHC was correlated with [18F]FAZIN3 binding. All PD brains were positively UIHC stained and confirmed presence of LB. Outer cortical layers (I–III) of PD AC had 21% UIHC while inner layers (IV–VI) had >75% UIHC. In the CN brains LB were absent (<1% UIHC). Increased [18F]FAZIN3 binding to MAO-A in AC was observed in all PD subjects. [18F]FAZIN3 ratio in PD was AC/CC = 3.57 while in CN subjects it was AC/CC = 2.24. Increases in UIHC μm2 correlated with [18F]FAZIN3 binding to MAO-A in DLU/mm2. Increased [18F]FAZIN3 binding to MAO-A in PD is a potential novel “hot spot” PET imaging approach. Full article
(This article belongs to the Special Issue Experimental Diagnostics and Therapeutics in Parkinson’s Disease)
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18 pages, 4043 KiB  
Article
Rifaximin Modifies Gut Microbiota and Attenuates Inflammation in Parkinson’s Disease: Preclinical and Clinical Studies
by Chien-Tai Hong, Lung Chan, Kai-Yun Chen, Hsun-Hua Lee, Li-Kai Huang, Yu-Chen S. H. Yang, Yun-Ru Liu and Chaur-Jong Hu
Cells 2022, 11(21), 3468; https://doi.org/10.3390/cells11213468 - 02 Nov 2022
Cited by 11 | Viewed by 2906
Abstract
Patients with Parkinson’s disease (PD) exhibit distinct gut microbiota, which may promote gut-derived inflammation. Rifaximin is a nonabsorbable antibiotic that can modify gut microbiota. The present study investigated the effect of rifaximin on gut microbiota and inflammation status in PD. The study examined [...] Read more.
Patients with Parkinson’s disease (PD) exhibit distinct gut microbiota, which may promote gut-derived inflammation. Rifaximin is a nonabsorbable antibiotic that can modify gut microbiota. The present study investigated the effect of rifaximin on gut microbiota and inflammation status in PD. The study examined the effect of long-term rifaximin treatment on in vivo transgenic PD mice (MitoPark) and short-term rifaximin treatment on patients with PD. Rifaximin treatment caused a significant change in gut microbiota in the transgenic PD mice; in particular, it reduced the relative abundance of Prevotellaceae UCG-001 and increased the relative abundance of Bacteroides, Muribaculum, and Lachnospiraceae UCG-001. Rifaximin treatment attenuated serum interleukin-1β, interleukin-6 and tumor necrosis factor-α, claudin-5 and occludin, which indicated the reduction of systemic inflammation and the protection of the blood–brain barrier integrity. The rifaximin-treated MitoPark mice exhibited better motor and memory performance than did the control mice, with lower microglial activation and increased neuronal survival in the hippocampus. In the patients with PD, 7-day rifaximin treatment caused an increase in the relative abundance of Flavonifractor 6 months after treatment, and the change in plasma proinflammatory cytokine levels was negatively associated with the baseline plasma interleukin-1α level. In conclusion, the present study demonstrated that rifaximin exerted a neuroprotective effect on the transgenic PD mice by modulating gut microbiota. We observed that patients with higher baseline inflammation possibly benefited from rifaximin treatment. With consideration for the tolerability and safety of rifaximin, randomized controlled trials should investigate the disease-modification effect of long-term treatment on select patients with PD. Full article
(This article belongs to the Special Issue Experimental Diagnostics and Therapeutics in Parkinson’s Disease)
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18 pages, 3149 KiB  
Article
Parkinson’s Disease-Specific Autoantibodies against the Neuroprotective Co-Chaperone STIP1
by Jolene Su Yi Tan, Bernett Lee, Jackwee Lim, Dong Rui Ma, Jia Xin Goh, Suh Yee Goh, Muhammad Yaaseen Gulam, Ser Mei Koh, Weiling Wendy Lee, Lei Feng, Qing Wang, Yinxia Chao, Olaf Rötzschke and Eng King Tan
Cells 2022, 11(10), 1649; https://doi.org/10.3390/cells11101649 - 16 May 2022
Cited by 5 | Viewed by 5777
Abstract
Parkinson’s disease (PD) is a debilitating movement disorder characterised by the loss of dopaminergic neurons in the substantia nigra. As neuroprotective agents mitigating the rate of neurodegeneration are unavailable, the current therapies largely focus only on symptomatic relief. Here, we identified stress-inducible phosphoprotein [...] Read more.
Parkinson’s disease (PD) is a debilitating movement disorder characterised by the loss of dopaminergic neurons in the substantia nigra. As neuroprotective agents mitigating the rate of neurodegeneration are unavailable, the current therapies largely focus only on symptomatic relief. Here, we identified stress-inducible phosphoprotein 1 (STIP1) as a putative neuroprotective factor targeted by PD-specific autoantibodies. STIP1 is a co-chaperone with reported neuroprotective capacities in mouse Alzheimer’s disease and stroke models. With human dopaminergic neurons derived from induced pluripotent stem cells, STIP1 was found to alleviate staurosporine-induced neurotoxicity. A case-control study involving 50 PD patients (average age = 62.94 ± 8.48, Hoehn and Yahr >2 = 55%) and 50 age-matched healthy controls (HCs) (average age = 63.1 ± 8) further revealed high levels of STIP1 autoantibodies in 20% of PD patients compared to 10% of HCs. Using an overlapping peptide library covering the STIP1 protein, we identified four PD-specific B cell epitopes that were not recognised in HCs. All of these epitopes were located within regions crucial for STIP1’s chaperone function or prion protein association. Our clinical and neuro-immunological studies highlight the potential of the STIP1 co-chaperone as an endogenous neuroprotective agent in PD and suggest the possible involvement of autoimmune mechanisms via the production of autoantibodies in a subset of individuals. Full article
(This article belongs to the Special Issue Experimental Diagnostics and Therapeutics in Parkinson’s Disease)
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Review

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27 pages, 5244 KiB  
Review
Iron Brain Menace: The Involvement of Ferroptosis in Parkinson Disease
by Kai-Jung Lin, Shang-Der Chen, Kai-Lieh Lin, Chia-Wei Liou, Min-Yu Lan, Yao-Chung Chuang, Pei-Wen Wang, Jong-Jer Lee, Feng-Sheng Wang, Hung-Yu Lin and Tsu-Kung Lin
Cells 2022, 11(23), 3829; https://doi.org/10.3390/cells11233829 - 29 Nov 2022
Cited by 17 | Viewed by 3420
Abstract
Parkinson disease (PD) is the second-most common neurodegenerative disease. The characteristic pathology of progressive dopaminergic neuronal loss in people with PD is associated with iron accumulation and is suggested to be driven in part by the novel cell death pathway, ferroptosis. A unique [...] Read more.
Parkinson disease (PD) is the second-most common neurodegenerative disease. The characteristic pathology of progressive dopaminergic neuronal loss in people with PD is associated with iron accumulation and is suggested to be driven in part by the novel cell death pathway, ferroptosis. A unique modality of cell death, ferroptosis is mediated by iron-dependent phospholipid peroxidation. The mechanisms of ferroptosis inhibitors enhance antioxidative capacity to counter the oxidative stress from lipid peroxidation, such as through the system xc−/glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis and the coenzyme Q10 (CoQ10)/FSP1 pathway. Another means to reduce ferroptosis is with iron chelators. To date, there is no disease-modifying therapy to cure or slow PD progression, and a recent topic of research seeks to intervene with the development of PD via regulation of ferroptosis. In this review, we provide a discussion of different cell death pathways, the molecular mechanisms of ferroptosis, the role of ferroptosis in blood–brain barrier damage, updates on PD studies in ferroptosis, and the latest progress of pharmacological agents targeting ferroptosis for the intervention of PD in clinical trials. Full article
(This article belongs to the Special Issue Experimental Diagnostics and Therapeutics in Parkinson’s Disease)
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