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Mitochondrial dysfunction in Parkinson's disease
Open accessAbstract
Mitochondria are highly dynamic organelles which fulfill a plethora of functions. In addition to their prominent role in energy metabolism, mitochondria are intimately involved in various key cellular processes, such as the regulation of calcium homeostasis, stress response and cell death pathways. Thus, it is not surprising that an impairment of mitochondrial function results in cellular damage and is linked to aging and neurodegeneration. Many lines of evidence suggest that mitochondrial dysfunction plays a central role in the pathogenesis of Parkinson's disease (PD), starting in the early 1980s with the observation that an inhibitor of complex I of the electron transport chain can induce parkinsonism. Remarkably, recent research indicated that several PD-associated genes interface with pathways regulating mitochondrial function, morphology, and dynamics. In fact, sporadic and familial PD seem to converge at the level of mitochondrial integrity.
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“Recessively inherited loss-of-function mutations in PTEN-induced kinase 1 (PINK1) and the E3 ubiquitin ligase PRKN are the most common genetic causes for early-onset PD, which occurs in about 5%–10% of cases [1, 2].”
From miRNA family miR-29 inhibits PINK1-PRKN signaling via ATG9A (2026) · cites this paper as [2]
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“Loss-of-function mutations in the genes encoding PINK1 and PRKN result in early-onset Parkinson disease (EOPD).”
From miRNA family miR-29 inhibits PINK1-PRKN signaling via ATG9A (2026) · cites this paper as [2]
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“α-Synuclein has been reported to cause dysfunction of mitochondrial complex I in PD which in turn increases levels of ROS and consequently ROS-induced oxidative stress (Winklhofer and Haass 2010).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Winklhofer and Haass 2010
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Metadata
- Authors
- Winklhofer, K. F., & Haass, C.
- Affiliations
- German Center for Neurodegenerative Diseases (DE)
- Corresponding author
- Winklhofer, Konstanze F.
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 1802
- Issue
- 1
- Pages
- 29-44
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W2130497877
- Cited by
- 688
- References
- 326
- Citations by year
- 2026: 10 · 2025: 16 · 2024: 13 · 2023: 27 · 2022: 30 · 2021: 37 · 2020: 55 · 2019: 38 · 2018: 72 · 2017: 51 · 2016: 61 · 2015: 39 · 2014: 29 · 2013: 37 · 2012: 49
- FWCI
- 5.83
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Trinity's Access to Research Output (TARA) (Trinity College Dublin) (submittedVersion)
- Funders
- Deutsche Forschungsgemeinschaft (SFB 596)
- German Ministry for Education and Research
- the Helmholtz Alliance “Mental Health in an Ageing Society,”
- the Center for Integrated Protein Science Munich
- the Hans and Ilse Breuer Foundation
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dysfunction, Parkinson's disease, mitochondrial dynamics, mitochondrial morphology, mitochondrial complex I inhibition, parkinsonism, electron transport chain, calcium homeostasis, stress response, cell death pathways, neurodegeneration, aging, familial Parkinson's disease, sporadic Parkinson's disease
- MeSH terms
- Animals, DNA, Mitochondrial, Humans, Mitochondria, Models, Biological, Parkinson Disease, Oxidative Stress, Mitochondrial Proteins
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