Mitochondrial Dysfunction in Parkinson's Disease

By P. Keane, M. Kurzawa, P. Blain, Christopher M Morris. Parkinson's Disease, 2011

1,001 citations recorded by the source corpus.

Parkinson's disease (PD) is a progressive, neurodegenerative condition that has increasingly been linked with mitochondrial dysfunction and inhibition of the electron transport chain. This inhibition leads to the generation of reactive oxygen species and depletion of cellular energy levels, which can consequently cause cellular damage and death mediated by oxidative stress and excitotoxicity. A number of genes that have been shown to have links with inherited forms of PD encode mitochondrial proteins or proteins implicated in mitochondrial dysfunction, supporting the central involvement of mitochondria in PD. This involvement is corroborated by reports that environmental toxins that inhibit the mitochondrial respiratory chain have been shown to be associated with PD. This paper aims to illustrate the considerable body of evidence linking mitochondrial dysfunction with neuronal cell death in the substantia nigra pars compacta (SNpc) of PD patients and to highlight the important need for further research in this area.

Subfields: Cellular and Molecular Neuroscience, Neurology

View Paper: https://www.semanticscholar.org/paper/ad54fa57e37da9afb5b3294a8e8a14061ff134c4

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. A. Schapira
3. M. Mouradian
4. O. Maier
5. Roman Fischer
6. V. Dias
7. E. Junn

In Neurology

1. P. Jenner
2. M. Mouradian
3. V. Dias
4. E. Junn
5. A. Schapira
6. O. Maier
7. Roman Fischer
8. D. Dexter

Citations in the corpus

• Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences (2012, neutral): “…(reviewed in Abou-Sleiman et al , 2006; Lin and Beal, 2006; Mandemakers et al , 2007; Bogaerts et al , 2008; Henchcliffe and Beal, 2008; Schapira, 2008; Vila et al , 2008; Van Laar and Berman, 2009; Bueler, 2010; Burbulla et al , 2010; Winklhofer and Haass, 2010; and Schon and Przedborski, 2011).”
• The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “Therefore, impairment of mitochondrial function leads to cellular damage and is related to neurodegeneration [4].”
• Interrelation of Oxidative Stress and Inflammation in Neurodegenerative Disease: Role of TNF (2015, background): “Both Aβ and α-synuclein can directly activate NOX2 in microglia causing a burst of superoxide [32, 63].”
• Metals, oxidative stress and neurodegenerative disorders (2010, neutral): “PINK1 is an N-terminal mitochondrial targeting sequence and a serine/threonine kinase domain containing 581 amino acids [104].”
• Etiology and pathogenesis of Parkinson's disease (2011, background): “Several expression or knockout models of these mutations have been found to have defects of mitochondrial function.(47) Parkin is ubiquitously transcribed, and intracellular localization studies have described association of the parkin protein with the endoplasmic reticulum, Golgi apparatus, synapti”
• The Role of Oxidative Stress in Neurodegenerative Diseases (2015, background): “Parkinson’s disease (PD) is a neurodegenerative disorder characterized by selective neuronal loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc) and decreased DA levels in the nigrostriatal DA pathway in the brain [85, 86].”