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The Mechanism of Dopaminergic Neuron Degeneration/Survival

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 August 2021) | Viewed by 11116

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Special Issue Editors

Dr. Ana I. Rodríguez-Pérez

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Guest Editor

1. Research Center for Molecular Medicine and Chronic Diseases (CIMUS), IDIS, University of Santiago de Compostela, 15782 Santiago de Compostela, Spain
2. Networking Research Center on Neurodegenerative Diseases (CIBERNED), 28031 Madrid, Spain
Interests: neurodegeneration; Parkinson’s disease; renin-angiotensin system
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Dr. Rita Valenzuela

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Guest Editor

Universidad de Santiago de Compsotela, Santiago de Compostela, Spain
Interests: neurodegeneration; neuroinflammation; oxidative stress; Parkinson´s disease; aging; dopamine; mitochondrial dysfunction

Special Issue Information

We are delighted to announce a call for submissions to a Special Issue of the International Journal of Molecular Sciences on the topic of ‘’The Mechanism of Dopaminergic Neuron Degeneration/Survival’’.

Progressive degeneration of dopaminergic neurons in the substantia nigra pars compacta, and the subsequent loss of neurotransmitter dopamine in the striatum, causes the major clinical symptoms in Parkinson´s disease. This neurological disorder produces an important disability to the patient who suffers from it, being the fastest growing of neurological disorders in the word. As life expectancy increases, the number of patients with Parkinson’s disease is growing exponentially, and it is becoming a major health, social and economic challenge.

In this Special Issue, we will discuss some important aspects of dopaminergic degeneration, such as mechanisms of progression, new methods for degeneration study, the discovery of new biomarkers for the early detection of the disease, the use of different neuroprotective therapies and the clinical implications of dopaminergic degeneration.

We encourage the submission of both original research articles and topical reviews on all aspects of the ‘’Mechanism of Dopaminergic Neuron Degeneration/Survival’’. All submitted articles will undergo peer review.

Dr. Ana I. Rodríguez-Pérez
Dr. Rita Valenzuela
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.

Keywords

neurodegeneration
neuroinflammation
oxidative stress
Parkinson´s disease
aging
dopamine
mitochondrial dysfunction
synuclein
neuroprotection

Published Papers (3 papers)

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Research

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18 pages, 4257 KiB

Open AccessArticle

L-dopa-Dependent Effects of GLP-1R Agonists on the Survival of Dopaminergic Cells Transplanted into a Rat Model of Parkinson Disease

by Osama F. Elabi, Jeffrey S. Davies and Emma L. Lane

Int. J. Mol. Sci. 2021, 22(22), 12346; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222212346 - 16 Nov 2021

Cited by 3 | Viewed by 2397

Abstract

Cell therapy is a promising treatment for Parkinson’s disease (PD), however clinical trials to date have shown relatively low survival and significant patient-to-patient variability. Glucagon Like Peptide-1 receptor (GLP-1R) agonists have potential neuroprotective effects on endogenous dopaminergic neurons. This study explores whether these agents could similarly support the growth and survival of newly transplanted neurons. 6-OHDA lesioned Sprague Dawley rats received intra-striatal grafts of dopaminergic ventral mesencephalic cells from embryonic day 14 Wistar rat embryos. Transplanted rats then received either saline or L-dopa (12 mg/kg) administered every 48 h prior to, and following cell transplantation. Peripheral GLP-1R agonist administration (exendin-4, 0.5 μg/kg twice daily or liraglutide, 100 μg/kg once daily) commenced immediately after cell transplantation and was maintained throughout the study. Graft survival increased under administration of exendin-4, with motor function improving significantly following treatment with both exendin-4 and liraglutide. However, this effect was not observed in rats administered with L-dopa. In contrast, L-dopa treatment with liraglutide increased graft volume, with parallel increases in motor function. However, this improvement was accompanied by an increase in leukocyte infiltration around the graft. The co-administration of L-dopa and exendin-4 also led to indicators of insulin resistance not seen with liraglutide, which may underpin the differential effects observed between the two GLP1-R agonists. Overall, there may be some benefit to the supplementation of grafted patients with GLP-1R agonists but the potential interaction with other pharmacological treatments needs to be considered in more depth. Full article

(This article belongs to the Special Issue The Mechanism of Dopaminergic Neuron Degeneration/Survival)

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21 pages, 2995 KiB

Open AccessArticle

Loliolide, a New Therapeutic Option for Neurological Diseases? In Vitro Neuroprotective and Anti-Inflammatory Activities of a Monoterpenoid Lactone Isolated from Codium tomentosum

by Joana Silva, Celso Alves, Alice Martins, Patrícia Susano, Marco Simões, Miguel Guedes, Stephanie Rehfeldt, Susete Pinteus, Helena Gaspar, Américo Rodrigues, Márcia Ines Goettert, Amparo Alfonso and Rui Pedrosa

Int. J. Mol. Sci. 2021, 22(4), 1888; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22041888 - 14 Feb 2021

Cited by 33 | Viewed by 4239

Abstract

Parkinsons Disease (PD) is the second most common neurodegenerative disease worldwide, and is characterized by a progressive degeneration of dopaminergic neurons. Without an effective treatment, it is crucial to find new therapeutic options to fight the neurodegenerative process, which may arise from marine resources. Accordingly, the goal of the present work was to evaluate the ability of the monoterpenoid lactone Loliolide, isolated from the green seaweed Codium tomentosum, to prevent neurological cell death mediated by the neurotoxin 6-hydroxydopamine (6-OHDA) on SH-SY5Y cells and their anti-inflammatory effects in RAW 264.7 macrophages. Loliolide was obtained from the diethyl ether extract, purified through column chromatography and identified by NMR spectroscopy. The neuroprotective effects were evaluated by the MTT method. Cells’ exposure to 6-OHDA in the presence of Loliolide led to an increase of cells’ viability in 40%, and this effect was mediated by mitochondrial protection, reduction of oxidative stress condition and apoptosis, and inhibition of the NF-kB pathway. Additionally, Loliolide also suppressed nitric oxide production and inhibited the production of TNF-α and IL-6 pro-inflammatory cytokines. The results suggest that Loliolide can inspire the development of new neuroprotective therapeutic agents and thus, more detailed studies should be considered to validate its pharmacological potential. Full article

(This article belongs to the Special Issue The Mechanism of Dopaminergic Neuron Degeneration/Survival)

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Review

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20 pages, 5666 KiB

Open AccessReview

Dual Roles of Microglia in the Basal Ganglia in Parkinson’s Disease

by Mohammed E. Choudhury, Yuka Kigami and Junya Tanaka

Int. J. Mol. Sci. 2021, 22(8), 3907; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22083907 - 09 Apr 2021

Cited by 8 | Viewed by 3787

Abstract

With the increasing age of the population, the incidence of Parkinson’s disease (PD) has increased exponentially. The development of novel therapeutic interventions requires an understanding of the involvement of senescent brain cells in the pathogenesis of PD. In this review, we highlight the roles played by microglia in the basal ganglia in the pathophysiological processes of PD. In PD, dopaminergic (DAergic) neuronal degeneration in the substantia nigra pars compacta (SNc) activates the microglia, which then promote DAergic neuronal degeneration by releasing potentially neurotoxic factors, including nitric oxide, cytokines, and reactive oxygen species. On the other hand, microglia are also activated in the basal ganglia outputs (the substantia nigra pars reticulata and the globus pallidus) in response to excess glutamate released from hyperactive subthalamic nuclei-derived synapses. The activated microglia then eliminate the hyperactive glutamatergic synapses. Synapse elimination may be the mechanism underlying the compensation that masks the appearance of PD symptoms despite substantial DAergic neuronal loss. Microglial senescence may correlate with their enhanced neurotoxicity in the SNc and the reduced compensatory actions in the basal ganglia outputs. The dual roles of microglia in different basal ganglia regions make it difficult to develop interventions targeting microglia for PD treatment. Full article

(This article belongs to the Special Issue The Mechanism of Dopaminergic Neuron Degeneration/Survival)

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