ParkinsonCanadaV1, Main, Exploration, bibRecord, 000646

Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.

Identifieur interne : 000646 ( Main/Exploration ); précédent : 000645; suivant : 000647

Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.

Auteurs : Brent J. Ryan [Royaume-Uni] ; Selim Hoek [Royaume-Uni] ; Edward A. Fon [Canada] ; Richard Wade-Martins [Royaume-Uni]

Source :

Trends in biochemical sciences [ 0968-0004 ] ; 2015.

RBID : pubmed:25757399

English descriptors

KwdEn :
- Animals, Humans, Mitochondria (metabolism), Mitochondria (pathology), Parkinson Disease (metabolism), Parkinson Disease (pathology), alpha-Synuclein (metabolism).
MESH :
- chemical , metabolism : alpha-Synuclein.
- metabolism : Mitochondria, Parkinson Disease.
- pathology : Mitochondria, Parkinson Disease.
- Animals, Humans.

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the preferential loss of dopaminergic neurons in the substantia nigra. Mitochondrial dysfunction is increasingly appreciated as a key determinant of dopaminergic neuronal susceptibility in PD and is a feature of both familial and sporadic disease, as well as in toxin-induced Parkinsonism. Recently, the mechanisms by which PD-associated mitochondrial proteins phosphatase and tensin homolog deleted on chromosome 10 (PTEN)-induced putative kinase 1 (PINK1) and parkin function and induce neurodegeneration have been identified. In addition, increasing evidence implicates other PD-associated proteins such as α-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) in mitochondrial dysfunction in genetic cases of PD with the potential for a large functional overlap with sporadic disease. This review highlights how recent advances in understanding familial PD-associated proteins have identified novel mechanisms and therapeutic strategies for addressing mitochondrial dysfunction in PD.

DOI: 10.1016/j.tibs.2015.02.003
PubMed: 25757399

Affiliations:

Le document en format XML

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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a progressive neurodegenerative disorder characterised by the preferential loss of dopaminergic neurons in the substantia nigra. Mitochondrial dysfunction is increasingly appreciated as a key determinant of dopaminergic neuronal susceptibility in PD and is a feature of both familial and sporadic disease, as well as in toxin-induced Parkinsonism. Recently, the mechanisms by which PD-associated mitochondrial proteins phosphatase and tensin homolog deleted on chromosome 10 (PTEN)-induced putative kinase 1 (PINK1) and parkin function and induce neurodegeneration have been identified. In addition, increasing evidence implicates other PD-associated proteins such as α-synuclein (α-syn) and leucine-rich repeat kinase 2 (LRRK2) in mitochondrial dysfunction in genetic cases of PD with the potential for a large functional overlap with sporadic disease. This review highlights how recent advances in understanding familial PD-associated proteins have identified novel mechanisms and therapeutic strategies for addressing mitochondrial dysfunction in PD.</div>
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La maladie de Parkinson au Canada (serveur d'exploration)

Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.

Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.

Source :

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki

	La maladie de Parkinson au Canada (serveur d'exploration)
	Attention, ce site est en cours de développement ! Attention, site généré par des moyens informatiques à partir de corpus bruts. Les informations ne sont donc pas validées.