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Neuroinflammation in Parkinson's Disease
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Neuroinflammation in Parkinson's Disease

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: closed (30 June 2022) | Viewed by 3145

Special Issue Editor

Dr. Juliet M. Taylor

E-Mail Website
Guest Editor
Department of Pharmacology and Therapeutics, The University of Melbourne, Victoria 3010, Australia
Interests: neuroinflammation; type-I interferons; Parkinson’s disease; microglia; Alzheimer’s disease

Special Issue Information

Dear Colleagues,

Parkinson’s disease (PD) is a chronic neurodegenerative disease characterised by motor dysfunction due to a loss of dopaminergic neurons.  It is considered a multifactorial disorder promoted by both genetic defects and exposure to environmental factors influencing disease progression. Recent clinical, epidemiological and experimental evidence has implicated neuroinflammation in contributing to the neuronal cell death and progression of PD. This chronic neuroinflammatory response within the central nervous system is driven by the resident immune cells of the brain, the microglia and astrocytes; however, recent studies have identified an important contribution of the peripheral immune response to the CNS pathology in PD. This aim of this Special Issue is to gain a greater understanding of the complex molecular mechanisms that lead to chronic neuroinflammation in PD and how these contribute to the dopaminergic cell death in the brain. Both high-quality original research and review articles are welcome discussing the following: neuroinflammation in cell-based and animal models of PD, microglia and astrocytes in PD, the gut–brain axis, the role of the peripheral immune response, and the development of therapeutic strategies targeting neuroinflammation.

Dr. Juliet M. Taylor
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. 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

  • parkinson’s disease
  • neurodegenerative
  • neuroinflammation
  • microglia
  • astrocytes
  • gut-brain axis
  • alpha-synuclein
  • dopamine

Published Papers (1 paper)

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Research

11 pages, 1604 KiB  
Article
Diosgenin Prevents Microglial Activation and Protects Dopaminergic Neurons from Lipopolysaccharide-Induced Neural Damage In Vitro and In Vivo
by Shou-Lun Lee, Ssu-Chieh Tu, Ming-Yen Hsu and Ting-Yu Chin
Int. J. Mol. Sci. 2021, 22(19), 10361; https://doi.org/10.3390/ijms221910361 - 26 Sep 2021
Cited by 10 | Viewed by 2687
Abstract
Background: The prevention of age-related neurodegenerative disorders is an important issue in an aging society. Microglia-mediated neuroinflammation resulting in dopaminergic neuron loss may lead to the pathogenesis of Parkinson’s disease (PD). Lipopolysaccharide (LPS), an endotoxin, induces neuroinflammatory microglial activation, contributing to dopaminergic neuron [...] Read more.
Background: The prevention of age-related neurodegenerative disorders is an important issue in an aging society. Microglia-mediated neuroinflammation resulting in dopaminergic neuron loss may lead to the pathogenesis of Parkinson’s disease (PD). Lipopolysaccharide (LPS), an endotoxin, induces neuroinflammatory microglial activation, contributing to dopaminergic neuron damage. Diosgenin is a phytosteroid sapogenin with a wide spectrum of pharmacological activities, e.g., anti-inflammatory activity. However, the preventive effect of diosgenin on neuroinflammation is not clear. Thus, in this study, we further investigated the neuroprotective effect of diosgenin on LPS-induced neural damage in vitro and in vivo. Methods: For in vitro experiments, primary mesencephalic neuron-glia cultures and primary microglia cultures isolated from Sprague–Dawley rats were used. Cells were pretreated with diosgenin and then stimulated with LPS. The expression of proinflammatory cytokines or tyrosine hydroxylase (TH) in the cells was analyzed. In vivo, rats were fed a diet containing 0.1% (w/w) diosgenin for 4 weeks before being administered a unilateral substantia nigra (SN) injection of LPS. Four weeks after the LPS injection, the rats were assessed for lesion severity using the amphetamine-induced rotation test and TH immunohistochemistry. Results: Diosgenin pretreatment prevented LPS-induced neurite shortening in TH-positive neurons in mesencephalic neuron-glia cultures. In addition, pretreatment of primary microglia with diosgenin significantly reduced tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS) expression. Moreover, diosgenin pretreatment significantly suppressed LPS-induced extracellular signal-regulated kinase (ERK) activation. In vivo, the intranigral injection of LPS in rats fed a diosgenin-containing diet significantly improved motor dysfunction and reduced TH expression in SN. Conclusion: These results support the effectiveness of diosgenin in protecting dopaminergic neurons from LPS-induced neuroinflammation. Full article
(This article belongs to the Special Issue Neuroinflammation in Parkinson's Disease)
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