» Articles » PMID: 21461368

Mitochondrial Dysfunction in Parkinson's Disease

Overview
Journal Parkinsons Dis
Publisher Wiley
Date 2011 Apr 5
PMID 21461368
Citations 63
Authors
Affiliations
Soon will be listed here.
Abstract

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.

Citing Articles

Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson's Disease.

Salis Torres A, Lee J, Caporali A, Semple R, Horrocks M, Macrae V Int J Mol Sci. 2024; 25(20).

PMID: 39456761 PMC: 11507255. DOI: 10.3390/ijms252010973.


Neuroprotective Effects of Total Extract and Isolated Compounds.

Eltahir A, Omoruyi S, Augustine T, Luckay R, Hussein A Pharmaceuticals (Basel). 2024; 17(7).

PMID: 39065703 PMC: 11279424. DOI: 10.3390/ph17070852.


Escalating Bi-Directional Feedback Loops between Proinflammatory Microglia and Mitochondria in Ageing and Post-Diagnosis of Parkinson's Disease.

Ravenhill S, Evans A, Crewther S Antioxidants (Basel). 2023; 12(5).

PMID: 37237983 PMC: 10215182. DOI: 10.3390/antiox12051117.


An Efficient 2D Protocol for Differentiation of iPSCs into Mature Postmitotic Dopaminergic Neurons: Application for Modeling Parkinson's Disease.

Lebedeva O, Sharova E, Grekhnev D, Skorodumova L, Kopylova I, Vassina E Int J Mol Sci. 2023; 24(8).

PMID: 37108456 PMC: 10139404. DOI: 10.3390/ijms24087297.


Pink1-/- Rats Demonstrate Swallowing and Gastrointestinal Dysfunction in a Model of Prodromal Parkinson Disease.

Krasko M, Szot J, Lungova K, Rowe L, Leverson G, Kelm-Nelson C Dysphagia. 2023; 38(5):1382-1397.

PMID: 36949296 PMC: 10514238. DOI: 10.1007/s00455-023-10567-0.


References
1.
Devi L, Raghavendran V, Prabhu B, Avadhani N, Anandatheerthavarada H . Mitochondrial import and accumulation of alpha-synuclein impair complex I in human dopaminergic neuronal cultures and Parkinson disease brain. J Biol Chem. 2008; 283(14):9089-100. PMC: 2431021. DOI: 10.1074/jbc.M710012200. View

2.
Sechi G, Agnetti V, Piredda M, Canu M, Deserra F, Omar H . Acute and persistent parkinsonism after use of diquat. Neurology. 1992; 42(1):261-3. DOI: 10.1212/wnl.42.1.261. View

3.
Leroy E, Boyer R, Auburger G, Leube B, Ulm G, Mezey E . The ubiquitin pathway in Parkinson's disease. Nature. 1998; 395(6701):451-2. DOI: 10.1038/26652. View

4.
Dexter D, Carter C, Agid F, Agid Y, Lees A, Jenner P . Lipid peroxidation as cause of nigral cell death in Parkinson's disease. Lancet. 1986; 2(8507):639-40. DOI: 10.1016/s0140-6736(86)92471-2. View

5.
Dykens J . Isolated cerebral and cerebellar mitochondria produce free radicals when exposed to elevated CA2+ and Na+: implications for neurodegeneration. J Neurochem. 1994; 63(2):584-91. DOI: 10.1046/j.1471-4159.1994.63020584.x. View