Cited by 883Parkinson's Disease Mechanisms and TreatmentsNuclear Receptors and SignalingMitochondrial Function and Pathology

Mitochondria in the aetiology and pathogenesis of Parkinson's disease

Schapira, Anthony HV·2008·The Lancet Neurology

Abstract

Several biochemical abnormalities have been described in the brains of patients with Parkinson's disease (PD), including oxidative stress and mitochondrial dysfunction. The identification of specific gene mutations that cause PD has reinforced the relevance of oxidative stress and mitochondrial dysfunction in the familial and the sporadic forms of the disease. The proteins that are associated with familial PD--PTEN-induced putative kinase 1 (PINK1), DJ-1, alpha-synuclein, leucine-rich repeat kinase 2, and, possibly, parkin--are either mitochondrial proteins or are associated with mitochondria, and all interface with the pathways of oxidative stress and free radical damage. Insights into the aetiology and pathogenesis of PD provide hope that drugs or cocktails of drugs that might successfully intervene in the pathogenesis and slow the progression of the disease can be derived from the study of the converging rather than diverging pathways to cell dysfunction and death.

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Crossref · 10.1016/s1474-4422(07)70327-7

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  • Impairment of mitochondrial complex-I activity has been observed in the substantia nigra, platelets, and skeletal muscle of PD patients, in some but not all studies.

    “An impairment of mitochondrial complex-I activity has been observed in the substantia nigra (SN), platelets, and skeletal muscle of PD patients 1, 9-13, in some but not in all studies14, 15.”

    From Mitochondrial Approaches for Neuroprotection (2008) · cites this paper as [11]

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Authors
Schapira, A. H.
Affiliations
UCL Queen Square Institute of Neurology (GB)
Corresponding author
Schapira, Anthony HV
Venue
The Lancet Neurology
Publisher
Elsevier BV
Published
2008-01
Volume
7
Issue
1
Pages
97-109
ISSN
1474-4422 (ISSN-L)
OpenAlex
W2139233019
Cited by
883
References
166
Citations by year
2026: 26 · 2025: 31 · 2024: 25 · 2023: 27 · 2022: 42 · 2021: 40 · 2020: 49 · 2019: 35 · 2018: 54 · 2017: 55 · 2016: 45 · 2015: 42 · 2014: 47 · 2013: 56 · 2012: 59
FWCI
12.33
Type
journal article
Language
en
Open access
closed
Locations
  • The Lancet Neurology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
Parkinson's disease, mitochondria, mitochondrial dysfunction, oxidative stress, PINK1, DJ-1, alpha-synuclein, LRRK2, Parkin, familial Parkinson's disease, sporadic Parkinson's disease, genetic mutations, oxidative damage, neurodegeneration
MeSH terms
Animals, Humans, Models, Biological, Parkinson Disease, Mitochondrial Proteins, Mitochondrial Diseases

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