Mitochondria in the aetiology and pathogenesis of Parkinson's disease.

By A. Schapira. Lancet Neurology, 2008

839 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/4fccb9ffd9ee98954feeaff8847c4cbefcb64a82

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. P. Jenner
2. D. Dexter
3. R. Youle
4. S. Jin
5. A. Abramov
6. N. Pichaud
7. S. Gandhi
8. J. Ballard

In Neurology

1. R. Youle
2. Derek P. Narendra
3. S. Jin
4. P. Jenner
5. D. Dexter
6. M. Komatsu
7. M. Mouradian
8. V. Dias

Citations in the corpus

• Mitochondria, oxidative stress and neurodegeneration. (2012, background): “The substantia nigra of PD patients shows reduced activity of mitochondrial respiratory electron transport chain NADPH deydrogenase (complex I) and complex I inhibitors such as rotenone, MPTP and pesticides cause neurological changes similar to PD [51].”
• Mitofusin 1 and mitofusin 2 are ubiquitinated in a PINK1/parkin-dependent manner upon induction of mitophagy. (2010, background): “Deficiency of complex I activity of the mitochondrial electron transport chain (ETC) has been reported in the substantia nigra of PD brains (3), while complex I inhibitors such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and rotenone can induce parkinsonian features in humans and animal models (”
• The Role of Oxidative Stress in Neurodegenerative Diseases (2015, background): “Although the exact mechanism still remains unclear, oxidative stress has been considered as one of major pathophysiological mechanisms underlying PD [86, 87].”
• PINK1 stabilized by mitochondrial depolarization recruits Parkin to damaged mitochondria and activates latent Parkin for mitophagy (2010, background): “PINK1 functions in mitochondrial maintenance, suggesting that mito chondrial integrity is another key factor in disease patho genesis (Dodson and Guo, 2007; Schapira, 2008).”
• PINK1- and Parkin-mediated mitophagy at a glance (2012, background): “Oxidative stress and mitochondrial dysfunction have been associated with PD pathogenesis (reviewed by Arduino et al., 2011; Cardoso, 2011; Schapira, 2008).”
• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “Remarkably, in about 25% of PD patients analysed complex I activities were found to be reduced also in platelets (reviewed in Schapira, 2008).”
• The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “tive stress described below [186], other factors that”
• Etiology and pathogenesis of Parkinson's disease (2011, background): “The first description of mitochondrial dysfunction in idiopathic PD(3,4) provided not only a direct link between environmental mitochondrial toxins and PD, but also laid the foundation for what has become the major focus for pathogenesis in genetic PD.(5)”
• Oxidative Stress in Parkinson's Disease: A Mechanism of Pathogenic and Therapeutic Significance (2008, background): “Alternatively, hydroxyl radical formation may be increased by increased availability of superoxide anion and hydrogen peroxide from impaired oxidative phosphorylation in mitochondria, and there is good evidence that oxidative phosphorylation becomes increasingly inefficient in aging and in PD [22].”
• PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin (2010, background): “. Increased mitochondrial damage in the SN, particularly to mtDNA, has been associated with sporadic Parkinson disease”
• The energy cost of action potential propagation in dopamine neurons: clues to susceptibility in Parkinson's disease (2013, background): “…including mitochondrial dysfunction, protein mishandling, inflammation, oxidative stress, genetic and environmental factors, and normal ageing (Chan et al., 2007; Sulzer, 2007; Schapira, 2008; Gasser, 2010; Guzman et al., 2010; Martin et al., 2010; Obeso et al., 2010; Surmeier et al., 2010a,b).”