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The Path to Cure in Parkinson’s Disease: Novel Concepts on Mechanisms, Disease Modifying Treatment, and Prevention

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 April 2024) | Viewed by 3236

Special Issue Editors

Prof. Dr. Yehonatan Sharabi

E-Mail Website
Guest Editor
Head, Neuroautonomic Service, Chaim Sheba Medical Center, Tel-HaShomer, Israel and Sackler Faculty of Medicine, Tel Aviv University, 6997801 Tel Aviv, Israel
Interests: Parkinson's disease; Lewy bodies; autonomic medicine; catecholamines; neuroprotection; disease-modifying treatment
Prof. Dr. David S. Goldstein

E-Mail Website
Guest Editor
Autonomic Medicine Section, NINDS Intramural Research Program, National Institutes of Health, Bethesda, MD 20892, USA
Interests: Parkinson's disease; Lewy bodies; autonomic medicine; catecholamines; neuroprotection; disease-modifying treatment

Special Issue Information

Dear Colleagues,

For many years, treatment for Parkinson's disease has focused on ways to increase the availability of dopamine at its receptors in the striatum. The disadvantages of this approach are inherent, both due to the approach that focuses on symptomatic treatment only and due to the focus on one aspect of a complex disease - the movement disorder. In recent years much information has accumulated about the pathogenesis of the disease and the way in which the disease progresses anatomically and physiologically, with increasing attention to the involvement of non-motor systems in the disease. The vast fund of information allows and enables many researchers to design and try more advanced and sophisticated treatments that are aimed at addressing the underlying dysfunctions of the systems involved in the disease and finding therapeutic strategies that can slow and possibly even prevent the neurodegenerative process.

The purpose of this Special Issue is to compile key articles and reviews on cutting-edge basic and clinical research on this topic and to present advanced concepts that mark promising trends for the future ranging from preclinical to prodromal to advanced disease, with emphasis on disease-modifying strategies.

Prof. Dr. Yehonatan Sharabi
Prof. Dr. David S. Goldstein
Guest Editors

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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 (2 papers)

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Research

12 pages, 861 KiB  
Article
Dihydroxyphenylacetaldehyde Lowering Treatment Improves Locomotor and Neurochemical Abnormalities in the Rat Rotenone Model: Relevance to the Catecholaldehyde Hypothesis for the Pathogenesis of Parkinson’s Disease
by Rawan Khashab, Naama Gutman-Sharabi, Zehava Shabtai, Regev Landau, Reut Halperin, Tsviya Fay-Karmon, Avshalom Leibowitz and Yehonatan Sharabi
Int. J. Mol. Sci. 2023, 24(15), 12522; https://doi.org/10.3390/ijms241512522 - 07 Aug 2023
Cited by 1 | Viewed by 1112
Abstract
The catecholaldehyde hypothesis for the pathogenesis of Parkinson’s disease centers on accumulation of 3,4-dihydroxyphenylacetaldehyde (DOPAL) in dopaminergic neurons. To test the hypothesis, it is necessary to reduce DOPAL and assess if this improves locomotor abnormalities. Systemic administration of rotenone to rats reproduces the [...] Read more.
The catecholaldehyde hypothesis for the pathogenesis of Parkinson’s disease centers on accumulation of 3,4-dihydroxyphenylacetaldehyde (DOPAL) in dopaminergic neurons. To test the hypothesis, it is necessary to reduce DOPAL and assess if this improves locomotor abnormalities. Systemic administration of rotenone to rats reproduces the motor and central neurochemical abnormalities characterizing Parkinson’s disease. In this study, we used the monoamine oxidase inhibitor (MAOI) deprenyl to decrease DOPAL production, with or without the antioxidant N-acetylcysteine (NAC). Adult rats received subcutaneous vehicle, rotenone (2 mg/kg/day via a minipump), or rotenone with deprenyl (5 mg/kg/day i.p.) with or without oral NAC (1 mg/kg/day) for 28 days. Motor function tests included measures of open field activity and rearing. Striatal tissue was assayed for contents of dopamine, DOPAL, and other catechols. Compared to vehicle, rotenone reduced locomotor activity (distance, velocity and rearing); increased tissue DOPAL; and decreased dopamine concentrations and inhibited vesicular sequestration of cytoplasmic dopamine and enzymatic breakdown of cytoplasmic DOPAL by aldehyde dehydrogenase (ALDH), as indicated by DA/DOPAL and DOPAC/DOPAL ratios. The addition of deprenyl to rotenone improved all the locomotor indices, increased dopamine and decreased DOPAL contents, and corrected the rotenone-induced vesicular uptake and ALDH abnormalities. The beneficial effects were augmented when NAC was added to deprenyl. Rotenone evokes locomotor and striatal neurochemical abnormalities found in Parkinson’s disease, including DOPAL buildup. Administration of an MAOI attenuates these abnormalities, and NAC augments the beneficial effects. The results indicate a pathogenic role of DOPAL in the rotenone model and suggest that treatment with MAOI+NAC might be beneficial for Parkinson’s disease treatment. Full article
(This article belongs to the Special Issue The Path to Cure in Parkinson’s Disease: Novel Concepts on Mechanisms, Disease Modifying Treatment, and Prevention)
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19 pages, 2071 KiB  
Article
Optogenetic Globus Pallidus Stimulation Improves Motor Deficits in 6-Hydroxydopamine-Lesioned Mouse Model of Parkinson’s Disease
by Sonia Di Bisceglie Caballero, Aurelia Ces, Martine Liberge, Frederic Ambroggi, Marianne Amalric and Abdel-Mouttalib Ouagazzal
Int. J. Mol. Sci. 2023, 24(9), 7935; https://doi.org/10.3390/ijms24097935 - 27 Apr 2023
Viewed by 1591
Abstract
Excessive inhibition of the external globus pallidus (GPe) by striatal GABAergic neurons is considered a central mechanism contributing to motor symptoms of Parkinson’s disease (PD). While electrophysiological findings support this view, behavioral studies assessing the beneficial effects of global GPe activations are scarce [...] Read more.
Excessive inhibition of the external globus pallidus (GPe) by striatal GABAergic neurons is considered a central mechanism contributing to motor symptoms of Parkinson’s disease (PD). While electrophysiological findings support this view, behavioral studies assessing the beneficial effects of global GPe activations are scarce and the reported results are controversial. We used an optogenetic approach and the standard unilateral 6-hydroxydopamine nigrostriatal dopamine (DA) lesion model of PD to explore the effects of GPe photostimulation on motor deficits in mice. Global optogenetic GPe inhibition was used in normal mice to verify whether it reproduced the typical motor impairment induced by DA lesions. GPe activation improved ipsilateral circling, contralateral forelimb akinesia, locomotor hypoactivity, and bradykinesia in 6-OHDA-lesioned mice at ineffective photostimulation parameters (532 nm, 5 Hz, 3 mW) in normal mice. GPe photoinhibition (450 nm, 12 mW) had no effect on locomotor activity and forelimb use in normal mice. Bilateral photoinhibition (450 nm, 6 mW/side) reduced directed exploration and improved working memory performances indicating that recruitment of GPe in physiological conditions may depend on the behavioral task involved. Collectively, these findings shed new light on the functional role of GPe and suggest that it is a promising target for neuromodulatory restoration of motor deficits in PD. Full article
(This article belongs to the Special Issue The Path to Cure in Parkinson’s Disease: Novel Concepts on Mechanisms, Disease Modifying Treatment, and Prevention)
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