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Biomedicines
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Pathophysiological Mechanisms of Parkinson's Disease
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Pathophysiological Mechanisms of Parkinson's Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: closed (31 August 2024) | Viewed by 4985

Special Issue Editor

Dr. Eun-Young Lee

E-Mail Website
Guest Editor
Department of Health Care and Science, Dong-A University, Busan 49315, Republic of Korea
Interests: neural correlates of cognitive dysfunctions in Parkinson’s disease using EEG and MRI techniques; structural and functional brain changes in PD related to disease progression and/or dementia conversion or disease modifying factors; biomarker studies in neurodegenerative disorders and at-risk populations; effects of chronic heavy metal exposure on the development of neurodegenerative disorders

Special Issue Information

Dear Colleagues,

Parkinson's disease is a neurodegenerative disorder characterized by motor symptoms such as tremors, rigidity, and bradykinesia. Understanding the complex processes involved in the development and progression of Parkinson's disease is crucial for advancing our knowledge and developing targeted therapeutic strategies.

This Special Issue, "Pathophysiological Mechanisms of Parkinson's Disease", will publish original research in basic science and translational research that can contribute to a better understanding of pathophysiological mechanisms underlying Parkinson’s disease. This Special Issue is multidisciplinary and aims to promote progress in the etiology, genetics, molecular correlates, pathogenesis, pharmacology, psychophysiology, cognitive dysfunctions, and neuroimaging correlates of Parkinson’s disease.

Dr. Eun-Young Lee
Guest Editor

Manuscript Submission Information

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Keywords

  • Parkinson’s disease
  • pathogenesis
  • genetics
  • molecular correlates
  • pharmacology
  • cognitive dysfunctions
  • Parkinson’s disease dementia
  • psychophysiology
  • EEG
  • MRI

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Published Papers (4 papers)

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Research

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18 pages, 6764 KiB  
Article
Rotenone and Its Derivative, Rotenoisin A, Induce Neurodegeneration Differentially in SH-SY5Y Cells
by Mahesh Ramalingam, Sujeong Jang, Seongryul Kim, Hyoungwoo Bai, Gyeonghan Jeong, Byeong C. Kim and Han-Seong Jeong
Biomedicines 2024, 12(8), 1703; https://doi.org/10.3390/biomedicines12081703 - 31 Jul 2024
Viewed by 943
Abstract
Rotenone (ROT), the most significant rotenoid, which has shown anticancer activity, has also been reported to be toxic to normal cells, inducing Parkinson’s disease (PD)-like neuronal loss with aggregation of α-synuclein (α-syn). To reduce the adverse effects of ROT, its derivative, rotenoisin A [...] Read more.
Rotenone (ROT), the most significant rotenoid, which has shown anticancer activity, has also been reported to be toxic to normal cells, inducing Parkinson’s disease (PD)-like neuronal loss with aggregation of α-synuclein (α-syn). To reduce the adverse effects of ROT, its derivative, rotenoisin A (ROA), is obtained by directly irradiating a ROT solution in methanol using γ-rays, which has been reported for potential anticancer properties. However, its PD-inducing effects have not yet been researched or reported. This study sought to compare the activities of ROA and ROT on the aggregation of α-syn, apoptosis, and autophagy in SH-SY5Y cells. ROA decreased cell survival less when compared with ROT on SH-SY5Y cells at 48 h in a dose-dependent manner. ROT (0.5 and 1 μM) and ROA (4 and 5 μM) decreased the expression of tyrosine hydroxylase. Western blot analysis of the Triton X-100 insoluble fraction revealed that both ROT and ROA significantly increased the levels of oligomeric, dimeric, and monomeric phosphorylated Serine129 α-syn and total monomeric α-syn. Moreover, both compounds decreased the proportion of neuronal nuclei, the neurofilament-heavy chain, and β3-tubulin. The phosphorylation of ERK and SAPK were reduced, whereas ROA did not act on Akt. Additionally, the increased Bax/Bcl-2 ratio further activated the downstream caspases cascade. ROT promoted the LC3BII/I ratio and p62 levels; however, different ROA doses resulted in different effects on autophagy while inducing PD-like impairments in SH-SY5Y cells. Full article
(This article belongs to the Special Issue Pathophysiological Mechanisms of Parkinson's Disease)
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8 pages, 540 KiB  
Communication
Analysis of LRRN3, MEF2C, SLC22A, and P2RY12 Gene Expression in the Peripheral Blood of Patients in the Early Stages of Parkinson’s Disease
by Marina V. Shulskaya, Ekaterina I. Semenova, Margarita M. Rudenok, Suzanna A. Partevian, Maria V. Lukashevich, Alexei V. Karabanov, Ekaterina Yu. Fedotova, Sergey N. Illarioshkin, Petr A. Slominsky, Maria I. Shadrina and Anelya Kh. Alieva
Biomedicines 2024, 12(7), 1391; https://doi.org/10.3390/biomedicines12071391 - 23 Jun 2024
Viewed by 861
Abstract
Parkinson’s disease (PD) is one of the most common human neurodegenerative diseases. Belated diagnoses of PD and late treatment are caused by its elongated prodromal phase. Thus, searching for new candidate genes participating in the development of the pathological process in the early [...] Read more.
Parkinson’s disease (PD) is one of the most common human neurodegenerative diseases. Belated diagnoses of PD and late treatment are caused by its elongated prodromal phase. Thus, searching for new candidate genes participating in the development of the pathological process in the early stages of the disease in patients who have not yet received therapy is relevant. Changes in mRNA and protein levels have been described both in the peripheral blood and in the brain of patients with PD. Thus, analysis of changes in the mRNA expression in peripheral blood is of great importance in studying the early stages of PD. This work aimed to analyze the changes in MEF2C, SLC22A4, P2RY12, and LRRN3 gene expression in the peripheral blood of patients in the early stages of PD. We found a statistically relevant and PD-specific change in the expression of the LRRN3 gene, indicating a disruption in the processes of neuronal regeneration and the functioning of synapses. The data obtained during the study indicate that this gene can be considered a potential biomarker of the early stages of PD. Full article
(This article belongs to the Special Issue Pathophysiological Mechanisms of Parkinson's Disease)
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17 pages, 2915 KiB  
Article
Impaired Mitochondrial Network Morphology and Reactive Oxygen Species Production in Fibroblasts from Parkinson’s Disease Patients
by Kristina A. Kritskaya, Evgeniya I. Fedotova and Alexey V. Berezhnov
Biomedicines 2024, 12(2), 282; https://doi.org/10.3390/biomedicines12020282 - 25 Jan 2024
Cited by 2 | Viewed by 1750
Abstract
The mitochondrial network (MN) is a dynamic structure undergoing constant remodeling in the cell. It is assumed that perturbations to the MN may be associated with various pathologies, including Parkinson’s disease (PD). Using automatic image analysis and super-resolution microscopy, we have assessed the [...] Read more.
The mitochondrial network (MN) is a dynamic structure undergoing constant remodeling in the cell. It is assumed that perturbations to the MN may be associated with various pathologies, including Parkinson’s disease (PD). Using automatic image analysis and super-resolution microscopy, we have assessed the MN parameters in fibroblasts from patients with established hereditary PD mutations (associated with PINK1, LRRK2, and α-synuclein, as well as PINK1 and Parkin proteins simultaneously) under normal conditions and after hydrogen peroxide-induced stress. Fibroblasts with the Pink1/Parkin mutation are most different in morphology to fibroblasts obtained from conditionally healthy donors: the MN is larger, and it contains longer mitochondria and accumulated individual mitochondria. In addition to MN, we evaluated other cellular parameters, such as cytosolic and mitochondrial ROS production and mitochondrial membrane potential. It has been shown that mitochondria of fibroblasts with mutations in genes encoding PINK1, α-synuclein, and Pink/Parkin tend towards hyperpolarization and cytosolic ROS overproduction, while mitochondrial ROS production was higher only in fibroblasts with PINK1 and α-synuclein mutations. Full article
(This article belongs to the Special Issue Pathophysiological Mechanisms of Parkinson's Disease)
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Review

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13 pages, 1073 KiB  
Review
Current Perspectives on Olfactory Loss in Atypical Parkinsonisms—A Review Article
by Katarzyna Bochniak, Mateusz Soszyński, Natalia Madetko-Alster and Piotr Alster
Biomedicines 2024, 12(10), 2257; https://doi.org/10.3390/biomedicines12102257 - 4 Oct 2024
Viewed by 914
Abstract
Introduction: Atypical parkinsonisms (APs) present various symptoms including motor impairment, cognitive decline, and autonomic dysfunction. Olfactory loss (OL), being a significant non-motor symptom, has emerged as an under-evaluated, yet potentially valuable, feature that might aid in the differential diagnosis of APs. State of [...] Read more.
Introduction: Atypical parkinsonisms (APs) present various symptoms including motor impairment, cognitive decline, and autonomic dysfunction. Olfactory loss (OL), being a significant non-motor symptom, has emerged as an under-evaluated, yet potentially valuable, feature that might aid in the differential diagnosis of APs. State of the art: The most pronounced OL is usually associated with Dementia with Lewy Bodies (DLB). While the view about the normosmic course of Multiple System Atrophy (MSA) remains unchanged, research indicates that mild OL may occur in a subset of patients with Progressive Supranuclear Palsy (PSP) and Corticobasal Degeneration (CBD). This might be linked to the deposition of abnormal protein aggregates in the central nervous system. Clinical significance: The aim of this review is to discuss the role of OL and its degree and pattern in the pathogenesis and course of APs. Olfactory testing could serve as a non-invasive, quick screening tool to differentiate between APs and project disease progression. Future directions: There is a need for further evaluation of this topic. This may lead to the development of standardized olfactory testing protocols that could be implemented in clinical practice, making differential diagnosis of APs more convenient. Understanding differences in the sense of smell could create an avenue for more targeted therapeutic strategies. Full article
(This article belongs to the Special Issue Pathophysiological Mechanisms of Parkinson's Disease)
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