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

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...

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Main Authors: Ryan, B, Hoek, S, Fon, E, Wade-Martins, R
Format: Journal article
Language:English
Published: Elsevier 2015
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author Ryan, B
Hoek, S
Fon, E
Wade-Martins, R
author_facet Ryan, B
Hoek, S
Fon, E
Wade-Martins, R
author_sort Ryan, B
collection OXFORD
description 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.
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spelling oxford-uuid:a2dbf60e-828b-4f62-b5a2-036776e2882c2022-03-27T02:22:52ZMitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:a2dbf60e-828b-4f62-b5a2-036776e2882cEnglishSymplectic Elements at OxfordElsevier2015Ryan, BHoek, SFon, EWade-Martins, RParkinson'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.
spellingShingle Ryan, B
Hoek, S
Fon, E
Wade-Martins, R
Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.
title Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.
title_full Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.
title_fullStr Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.
title_full_unstemmed Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.
title_short Mitochondrial dysfunction and mitophagy in Parkinson's: from familial to sporadic disease.
title_sort mitochondrial dysfunction and mitophagy in parkinson s from familial to sporadic disease
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