Special Issue "Frontiers in Parkinson’s Disease (PD)"

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (10 November 2019).

Special Issue Editor

Dr. Alicia M. Pickrell
E-Mail Website
Guest Editor
School of Neuroscience, Virginia Polytechnic and State University, Blacksburg, VA 24061, USA
Interests: mitochondria; mitochondrial DNA; mitophagy; Parkinson’s disease; neurodegenerative diseases

Special Issue Information

Dear Colleagues,

Parkinson’s Disease (PD) is the most common motor deteriorating neurodegenerative disease with a majority of cases being sporadic in nature.  Over the past decade, researchers have begun to understand the physiological roles of different proteins that are mutated in monogenic forms of PD.  These insights provide information into what types of biological processes may go awry in sporadic PD and aid in our understanding of the pathophysiological changes occuring during degenerative processes. The effort of multiple research groups elucidated the mechanism by which PINK1 and Parkin (two genes mutated in recessive PD) target damaged mitochondria for autophagic removal. Recently, the substrates and phorphosylation sites for leucine-rich repeat kinase 2 (LRRK2) have been identified. LRRK2 is the gene most commonly mutated in autosomal dominant forms of PD.

Newly published large-scale genome wide association studies (GWAS) have identified risk loci and candidate genes that are also involved in PD.  It is imperitive that research efforts identify the function of these newly identified canidate genes (if unknown) and how these genes possibly contribute to neurodegeneration. The aim of this Special Issue, “Frontiers in Parkinson’s Disease,” is to encourage the publication of new experimental, translational and clinical findings to advance our understanding of the pathophysiological changes that occur in Parkinson’s Disease.

Assist. Prof. Alicia M. Pickrell
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 papers will be 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. Brain Sciences is an international peer-reviewed open access monthly 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 1400 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.

Keywords

  • Parkinson’s disease
  • Dopaminergic neurons
  • Neurodegeneration
  • Substantia nigra

Published Papers (3 papers)

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Research

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Open AccessArticle
Neuroprotective and Antioxidant Effect of Naringenin-Loaded Nanoparticles for Nose-to-Brain Delivery
Brain Sci. 2019, 9(10), 275; https://doi.org/10.3390/brainsci9100275 - 15 Oct 2019
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder resulting in a decreased nigrostriatal availability of dopamine. Oxidative stress is one factor contributing to PD. Naringenin (NAR), a flavonoid, is a potent antioxidant shown to be beneficial in experimental PD. The clinical development of NAR [...] Read more.
Parkinson’s disease (PD) is a neurodegenerative disorder resulting in a decreased nigrostriatal availability of dopamine. Oxidative stress is one factor contributing to PD. Naringenin (NAR), a flavonoid, is a potent antioxidant shown to be beneficial in experimental PD. The clinical development of NAR has been hampered due to its low bioavailability resulting from gastrointestinal degradation, inefficient permeability, and low aqueous solubility. The objective of the present research was to formulate and characterize naringenin-loaded chitosan nanoparticles (NAR NPs) for nose-to-brain delivery. The cellular uptake, cytotoxicity, and neuroprotective effects of NAR NPs were determined using the SH-SY5Y cell line in vitro. NAR NPs were prepared using the ionic gelation method and characterized by zetasizer, transmission electron microscopy (TEM), and field emission microscopy (FESEM). The average particle size, polydispersity index (PDI), zeta potential, entrapment efficiency, and 24 h in vitro release profile were 87.6 ± 8.47 nm, 0.31 ± 0.04, 15.36 ± 2.05 mV, 91.12 ± 2.99%, and 54.80 ± 4.22%, respectively. The percentage NAR permeation through nasal mucosa from NPs was found to be 67.90 ± 0.72%. Cellular uptake of prepared NPs was confirmed by fluorescence microscopy. Neuroprotective activity of NAR NPs was evaluated through viability assays and by estimating reactive oxygen species (ROS) levels. NAR NPs showed enhanced neuroprotective ability and antioxidant effect against 6-OHDA-induced neurotoxicity in SH-SY5Y cells. However, animal studies are necessary to establish the potential of NAR NPs to be an effective carrier for the treatment of PD for nose-to-brain delivery. Full article
(This article belongs to the Special Issue Frontiers in Parkinson’s Disease (PD))
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Review

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Open AccessReview
Postural Instability in Parkinson’s Disease: A Review
Brain Sci. 2019, 9(9), 239; https://doi.org/10.3390/brainsci9090239 - 18 Sep 2019
Abstract
Parkinson’s disease (PD) is a heterogeneous progressive neurodegenerative disorder, which typically affects older adults; it is predicted that by 2030 about 3% of the world population above 65 years of age is likely to be affected. At present, the diagnosis of PD is [...] Read more.
Parkinson’s disease (PD) is a heterogeneous progressive neurodegenerative disorder, which typically affects older adults; it is predicted that by 2030 about 3% of the world population above 65 years of age is likely to be affected. At present, the diagnosis of PD is clinical, subjective, nonspecific, and often inadequate. There is a need to quantify the PD factors for an objective disease assessment. Among the various factors, postural instability (PI) is unresponsive to the existing treatment strategies resulting in morbidity. In this work, we review the physiology and pathophysiology of postural balance that is essential to treat PI among PD patients. Specifically, we discuss some of the reported factors for an early PI diagnosis, including age, nervous system lesions, genetic mutations, abnormal proprioception, impaired reflexes, and altered biomechanics. Though the contributing factors to PI have been identified, how their quantification to grade PI severity in a patient can help in treatment is not fully understood. By contextualizing the contributing factors, we aim to assist the future research efforts that underpin posturographical and histopathological studies to measure PI in PD. Once the pathology of PI is established, effective diagnostic tools and treatment strategies could be developed to curtail patient falls. Full article
(This article belongs to the Special Issue Frontiers in Parkinson’s Disease (PD))
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Open AccessReview
Found in Translation: The Utility of C. elegans Alpha-Synuclein Models of Parkinson’s Disease
Brain Sci. 2019, 9(4), 73; https://doi.org/10.3390/brainsci9040073 - 28 Mar 2019
Cited by 1
Abstract
Parkinson’s Disease (PD) is the second-most common neurodegenerative disease in the world, yet the fundamental and underlying causes of the disease are largely unknown, and treatments remain sparse and impotent. Several biological systems have been employed to model the disease but the nematode [...] Read more.
Parkinson’s Disease (PD) is the second-most common neurodegenerative disease in the world, yet the fundamental and underlying causes of the disease are largely unknown, and treatments remain sparse and impotent. Several biological systems have been employed to model the disease but the nematode roundworm Caenorhabditis elegans (C. elegans) shows unique promise among these to disinter the elusive factors that may prevent, halt, and/or reverse PD phenotypes. Some of the most salient of these C. elegans models of PD are those that position the misfolding-prone protein alpha-synuclein (α-syn), a hallmark pathological component of PD, as the primary target for scientific interrogation. By transgenic expression of human α-syn in different tissues, including dopamine neurons and muscle cells, the primary cellular phenotypes of PD in humans have been recapitulated in these C. elegans models and have already uncovered multifarious genetic factors and chemical compounds that attenuate dopaminergic neurodegeneration. This review describes the paramount discoveries obtained through the application of different α-syn models of PD in C. elegans and highlights their established utility and respective promise to successfully uncover new conserved genetic modifiers, functional mechanisms, therapeutic targets and molecular leads for PD with the potential to translate to humans. Full article
(This article belongs to the Special Issue Frontiers in Parkinson’s Disease (PD))
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