Cited by 455Parkinson's Disease Mechanisms and TreatmentsMitochondrial Function and PathologyAutophagy in Disease and Therapy

Mitochondrial Dysfunction in Parkinson’s Disease

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Moon, Hyo Eun, Paek, Sun Ha·2015·Experimental Neurobiology

Abstract

Parkinson's disease (PD) is characterized by the selective loss of dopaminergic neurons of the substantia nigra pars compacta (SNc) with motor and nonmotor symptoms. Defective mitochondrial function and increased oxidative stress (OS) have been demonstrated as having an important role in PD pathogenesis, although the underlying mechanism is not clear. The etiopathogenesis of sporadic PD is complex with variable contributions of environmental factors and genetic susceptibility. Both these factors influence various mitochondrial aspects, including their life cycle, bioenergetic capacity, quality control, dynamic changes of morphology and connectivity (fusion, fission), subcellular distribution (transport), and the regulation of cell death pathways. Mitochondrial dysfunction has mainly been reported in various non-dopaminergic cells and tissue samples from human patients as well as transgenic mouse and fruit fly models of PD. Thus, the mitochondria represent a highly promising target for the development of PD biomarkers. However, the limited amount of dopaminergic neurons prevented investigation of their detailed study. For the first time, we established human telomerase reverse transcriptase (hTERT)-immortalized wild type, idiopathic and Parkin deficient mesenchymal stromal cells (MSCs) isolated from the adipose tissues of PD patients, which could be used as a good cellular model to evaluate mitochondrial dysfunction for the better understanding of PD pathology and for the development of early diagnostic markers and effective therapy targets of PD. In this review, we examine evidence for the roles of mitochondrial dysfunction and increased OS in the neuronal loss that leads to PD and discuss how this knowledge further improve the treatment for patients with PD.

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Authors
Moon, H. E., & Paek, S. H.
Affiliations
Seoul National University (KR)
Corresponding author
Paek, Sun Ha
Venue
Experimental Neurobiology
Published
2015-06-30
Volume
24
Issue
2
Pages
103-116
ISSN
  • 1226-2560 (ISSN-L)
  • 2093-8144
OpenAlex
W826091804
Cited by
455
References
95
Citations by year
2026: 52 · 2025: 62 · 2024: 57 · 2023: 50 · 2022: 44 · 2021: 33 · 2020: 39 · 2019: 25 · 2018: 35 · 2017: 27 · 2016: 27 · 2015: 4
FWCI
4.08
Type
journal article
Language
en
Open access
Locations
  • Experimental Neurobiology (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by-nc)
  • PubMed Central (publishedVersion, cc-by-nc)
  • PubMed (publishedVersion)
Funders
  • Korea Institute of Planning and Evaluation for Technology in Food, Agriculture, Forestry and Fisheries (311011-05-3-SB020)
  • Ministry of Health and Welfare (HI10C14110400, HI12C02050101, HI11C21100200)
  • Ministry of Trade, Industry and Energy (10050154)
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
Parkinson's disease, mitochondrial dysfunction, oxidative stress, dopaminergic neuron loss, substantia nigra pars compacta, mitochondrial dynamics, mitochondrial quality control, mitochondrial transport, cell death pathways, Parkin deficiency, mesenchymal stem cells, adipose tissue, genetic susceptibility, environmental risk factors

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