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Novel Concepts, New Perspectives, and Current Therapies for Parkinson’s Disease: 2nd Edition

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 February 2025 | Viewed by 5868

Special Issue Editor

Dr. Malgorzata Zaremba

E-Mail Website
Guest Editor
Department of Experimental and Clinical Pharmacology, Centre for Preclinical Research (CBP), The Medical University of Warsaw, Banacha 1B St., 02-097 Warsaw, Poland
Interests: Parkinson’s disease; therapy; drug; repurposing; novel compound; neurodegeneration; neuroinflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Parkinson’s disease (PD), the most common progressive, neurodegenerative movement disorder, is caused by a hypodopaminergic condition in the nigrostriatal system. Cardinal motor symptoms are the main determinant of the quality of life for those with PD, as well as the progression of the disability and possible nursing home placement. As life expectancy increases, the need for novel approaches to treat PD grows urgent. However, while most antiparkinsonian drugs offer symptomatic relief, they do not tackle the underlying etiology of the disease. In addition, there is currently no available therapy that slows down the progression of PD or even prevents its manifestation. The most significant limitations of approved drugs are mostly related to their side effects and lack of long-term efficacy. Therefore, driven by the increasing knowledge of neurodegeneration and neuroinflammation processes, extensive research efforts are underway to identify new strategies to modulate previously undruggable targets or to manage the disease.

The present Special Issue will highlight the state of current pharmacological strategies and explore drug candidates under treatment evaluation, as well as candidates for repurposing for the treatment of PD. Furthermore, this issue will also provide an overview of future studies and novel molecular targets that may be used to combat PD. Hence, for this Special Issue, we are inviting researchers to contribute original articles and reviews on these topics. Contributions from all research areas, including disease modeling, drug studies, and therapeutic interventions, are welcome.

I look forward to receiving your contributions.

Dr. Malgorzata Zaremba
Guest Editor

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Keywords

  • Parkinson’s disease
  • therapy
  • drug
  • repurposing
  • novel compound
  • neurodegeneration
  • neuroinflammation

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Related Special Issue

Published Papers (5 papers)

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Research

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19 pages, 1360 KiB  
Article
Non-Helicobacter pylori Helicobacters, a Treatable Provocateur of Parkinson’s Disease: Hypothesis, Evidence and Species Specificity
by Wenjing Wang, Melvyn Smith, Richard Ellis, Antonella Savio, Amanda Nevel, Chianna Umamahesan, Polychronis Pavlidis, Bu’ Hussain Hayee, David Taylor, Allan H. Young, André Charlett, Sylvia M. Dobbs and R. John Dobbs
Int. J. Mol. Sci. 2024, 25(23), 13123; https://doi.org/10.3390/ijms252313123 - 6 Dec 2024
Viewed by 555
Abstract
Epidemiological and eradication trial evidence indicates that Helicobacter pylori, a major causative factor in peptic ulcer and gastric cancer, is a driver of the hypokinesia of Parkinson’s disease (PD). Psychological (cognitive impairment, depression and anxiety) and gastrointestinal (peptic ulceration and constipation) PD [...] Read more.
Epidemiological and eradication trial evidence indicates that Helicobacter pylori, a major causative factor in peptic ulcer and gastric cancer, is a driver of the hypokinesia of Parkinson’s disease (PD). Psychological (cognitive impairment, depression and anxiety) and gastrointestinal (peptic ulceration and constipation) PD features can precede the symptomatic onset of motor features by decades. We hypothesise that the non-H. pylori Helicobacters (NHPH), which have farm, companion and wild animals as their main hosts, can have a role in PD aetiopathogenesis. In those occupationally at risk of NHPH infection, we address whether there is increased mortality with PD, or depression or suicide. Our systematic review gave evidence that occupational exposure to animals/their products is associated with excess mortality with PD. Indeed, whilst livestock farming increased the risk, crop farming decreased it. Moreover, excess mortality from non-Hodgkin lymphoma in livestock farmers is compatible with NHPH being causal. Our scoping review showed that farmers, veterinarians and abattoir workers have an increased risk of depression and suicide; whether their depression is associated with being down the pathway to PD and/or the presence of Helicobacter infection needs investigation. Regarding Helicobacter species specificity, the link between the presence of NHPH in gastric biopsy and PD was described using a ureA polymerase chain reaction (PCR) assay, targeting the most-commonly named NHPH, H. suis. We describe its redesign and optimisation as a probe-based PCR, confirming the exclusion of H. pylori but not H. suis specificity (additionally identifying 6 species of a 22-NHPH-species panel). The exploration of the zoonotic hypothesis requires a non-invasive pan-Helicobacter PCR screen, allowing the detection and molecular grouping of Helicobacter species. Full article
(This article belongs to the Special Issue Novel Concepts, New Perspectives, and Current Therapies for Parkinson’s Disease: 2nd Edition)
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13 pages, 735 KiB  
Article
Proximity Elongation Assay and ELISA for the Identification of Serum Diagnostic Biomarkers in Parkinson’s Disease and Progressive Supranuclear Palsy
by Costanza Maria Cristiani, Camilla Calomino, Luana Scaramuzzino, Maria Stella Murfuni, Elvira Immacolata Parrotta, Maria Giovanna Bianco, Giovanni Cuda, Aldo Quattrone and Andrea Quattrone
Int. J. Mol. Sci. 2024, 25(21), 11663; https://doi.org/10.3390/ijms252111663 - 30 Oct 2024
Viewed by 753
Abstract
Clinical differentiation of progressive supranuclear palsy (PSP) from Parkinson’s disease (PD) is challenging due to overlapping phenotypes and late onset of PSP specific symptoms, highlighting the need for easily assessable biomarkers. We used proximity elongation assay (PEA) to analyze 460 proteins in serum [...] Read more.
Clinical differentiation of progressive supranuclear palsy (PSP) from Parkinson’s disease (PD) is challenging due to overlapping phenotypes and late onset of PSP specific symptoms, highlighting the need for easily assessable biomarkers. We used proximity elongation assay (PEA) to analyze 460 proteins in serum samples from 46 PD, 30 PSP patients, and 24 healthy controls. ANCOVA was used to identify the most promising proteins and machine learning (ML) XGBoost and random forest algorithms to assess their classification performance. Promising proteins were also quantified by ELISA. Moreover, correlations between serum biomarkers and biological and clinical features were investigated. We identified five proteins (TFF3, CPB1, OPG, CNTN1, TIMP4) showing different levels between PSP and PD, which achieved good performance (AUC: 0.892) when combined by ML. On the other hand, when the three most significant biomarkers (TFF3, CPB1 and OPG) were analyzed by ELISA, there was no difference between groups. Serum levels of TFF3 positively correlated with age in all subjects’ groups, while for OPG and CPB1 such a correlation occurred in PSP patients only. Moreover, CPB1 positively correlated with disease severity in PD, while no correlations were observed in the PSP group. Overall, we identified CPB1 correlating with PD severity, which may support clinical staging of PD. In addition, our results showing discrepancy between PEA and ELISA technology suggest that caution should be used when translating proteomic findings into clinical practice. Full article
(This article belongs to the Special Issue Novel Concepts, New Perspectives, and Current Therapies for Parkinson’s Disease: 2nd Edition)
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28 pages, 8501 KiB  
Article
The Bifunctional Dimer Caffeine-Indan Attenuates α-Synuclein Misfolding, Neurodegeneration and Behavioral Deficits after Chronic Stimulation of Adenosine A1 Receptors
by Elisabet Jakova, Omozojie P. Aigbogun, Mohamed Taha Moutaoufik, Kevin J. H. Allen, Omer Munir, Devin Brown, Changiz Taghibiglou, Mohan Babu, Chris P. Phenix, Ed S. Krol and Francisco S. Cayabyab
Int. J. Mol. Sci. 2024, 25(17), 9386; https://doi.org/10.3390/ijms25179386 - 29 Aug 2024
Viewed by 1201
Abstract
We previously found that chronic adenosine A1 receptor stimulation with N6-Cyclopentyladenosine increased α-synuclein misfolding and neurodegeneration in a novel α-synucleinopathy model, a hallmark of Parkinson’s disease. Here, we aimed to synthesize a dimer caffeine-indan linked by a 6-carbon chain to cross [...] Read more.
We previously found that chronic adenosine A1 receptor stimulation with N6-Cyclopentyladenosine increased α-synuclein misfolding and neurodegeneration in a novel α-synucleinopathy model, a hallmark of Parkinson’s disease. Here, we aimed to synthesize a dimer caffeine-indan linked by a 6-carbon chain to cross the blood–brain barrier and tested its ability to bind α-synuclein, reducing misfolding, behavioral abnormalities, and neurodegeneration in our rodent model. Behavioral tests and histological stains assessed neuroprotective effects of the dimer compound. A rapid synthesis of the 18F-labeled analogue enabled Positron Emission Tomography and Computed Tomography imaging for biodistribution measurement. Molecular docking analysis showed that the dimer binds to α-synuclein N- and C-termini and the non-amyloid-β-component (NAC) domain, similar to 1-aminoindan, and this binding promotes a neuroprotective α-synuclein “loop” conformation. The dimer also binds to the orthosteric binding site for adenosine within the adenosine A1 receptor. Immunohistochemistry and confocal imaging showed the dimer abolished α-synuclein upregulation and aggregation in the substantia nigra and hippocampus, and the dimer mitigated cognitive deficits, anxiety, despair, and motor abnormalities. The 18F-labeled dimer remained stable post-injection and distributed in various organs, notably in the brain, suggesting its potential as a Positron Emission Tomography tracer for α-synuclein and adenosine A1 receptor in Parkinson’s disease therapy. Full article
(This article belongs to the Special Issue Novel Concepts, New Perspectives, and Current Therapies for Parkinson’s Disease: 2nd Edition)
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11 pages, 471 KiB  
Article
Serum Oligomeric α-Synuclein and p-tau181 in Progressive Supranuclear Palsy and Parkinson’s Disease
by Costanza Maria Cristiani, Luana Scaramuzzino, Andrea Quattrone, Elvira Immacolata Parrotta, Giovanni Cuda and Aldo Quattrone
Int. J. Mol. Sci. 2024, 25(13), 6882; https://doi.org/10.3390/ijms25136882 - 23 Jun 2024
Cited by 3 | Viewed by 1249
Abstract
Clinical differentiation of progressive supranuclear palsy (PSP) from Parkinson’s disease (PD) is challenging due to overlapping phenotypes and the late onset of specific atypical signs. Therefore, easily assessable diagnostic biomarkers are highly needed. Since PD is a synucleopathy while PSP is a tauopathy, [...] Read more.
Clinical differentiation of progressive supranuclear palsy (PSP) from Parkinson’s disease (PD) is challenging due to overlapping phenotypes and the late onset of specific atypical signs. Therefore, easily assessable diagnostic biomarkers are highly needed. Since PD is a synucleopathy while PSP is a tauopathy, here, we investigated the clinical usefulness of serum oligomeric-α-synuclein (o-α-synuclein) and 181Thr-phosphorylated tau (p-tau181), which are considered as the most important pathological protein forms in distinguishing between these two parkinsonisms. We assessed serum o-α-synuclein and p-tau181 by ELISA and SIMOA, respectively, in 27 PSP patients, 43 PD patients, and 39 healthy controls (HC). Moreover, we evaluated the correlation between serum biomarkers and biological and clinical features of these subjects. We did not find any difference in serum concentrations of p-tau181 and o-α-synuclein nor in the o-α-synuclein/p-tau181 ratio between groups. However, we observed that serum p-tau181 positively correlated with age in HC and PD, while serum o-α-synuclein correlated positively with disease severity in PD and negatively with age in PSP. Finally, the o-α-synuclein/p-tau181 ratio showed a negative correlation with age in PD. Full article
(This article belongs to the Special Issue Novel Concepts, New Perspectives, and Current Therapies for Parkinson’s Disease: 2nd Edition)
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Review

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28 pages, 2618 KiB  
Review
Hypoxia Pathways in Parkinson’s Disease: From Pathogenesis to Therapeutic Targets
by Yuanyuan Gao, Jiarui Zhang, Tuoxian Tang and Zhenjiang Liu
Int. J. Mol. Sci. 2024, 25(19), 10484; https://doi.org/10.3390/ijms251910484 - 29 Sep 2024
Cited by 1 | Viewed by 1704
Abstract
The human brain is highly dependent on oxygen, utilizing approximately 20% of the body’s oxygen at rest. Oxygen deprivation to the brain can lead to loss of consciousness within seconds and death within minutes. Recent studies have identified regions of the brain with [...] Read more.
The human brain is highly dependent on oxygen, utilizing approximately 20% of the body’s oxygen at rest. Oxygen deprivation to the brain can lead to loss of consciousness within seconds and death within minutes. Recent studies have identified regions of the brain with spontaneous episodic hypoxia, referred to as “hypoxic pockets”. Hypoxia can also result from impaired blood flow due to conditions such as heart disease, blood clots, stroke, or hemorrhage, as well as from reduced oxygen intake or excessive oxygen consumption caused by factors like low ambient oxygen, pulmonary diseases, infections, inflammation, and cancer. Severe hypoxia in the brain can manifest symptoms similar to Parkinson’s disease (PD), including cerebral edema, mood disturbances, and cognitive impairments. Additionally, the development of PD appears to be closely associated with hypoxia and hypoxic pathways. This review seeks to investigate the molecular interactions between hypoxia and PD, emphasizing the pathological role of hypoxic pathways in PD and exploring their potential as therapeutic targets. Full article
(This article belongs to the Special Issue Novel Concepts, New Perspectives, and Current Therapies for Parkinson’s Disease: 2nd Edition)
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