Cited by 690Parkinson's Disease Mechanisms and TreatmentsMitochondrial Function and PathologyAutophagy in Disease and Therapy

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Mitochondrial dysfunction in Parkinson's disease

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Winklhofer, Konstanze F., Haass, Christian·2010·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

DOI 10.1016/j.bbadis.2009.08.013

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Abstract

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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Authors: Winklhofer, K. F., & Haass, C.
Affiliations: German Center for Neurodegenerative Diseases (DE)
Corresponding author: Winklhofer, Konstanze F.
ORCID: Winklhofer, Konstanze F.
Haass, Christian
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)
DOI: 10.1016/j.bbadis.2009.08.013
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: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 1784 d)
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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Mitochondrial dysfunction in Parkinson's disease

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