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: 31 August 2024 | Viewed by 1124

Special Issue Editor


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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

Published Papers (1 paper)

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Research

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
Viewed by 932
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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