Understanding Dopaminergic Cell Death Pathways in Parkinson Disease
Identifieur interne : 000A73 ( Hal/Curation ); précédent : 000A72; suivant : 000A74Understanding Dopaminergic Cell Death Pathways in Parkinson Disease
Auteurs : Stéphane Hunot [France] ; Etienne Hirsch [France] ; Stéphane Hunot [France]Source :
- Neuron [ 0896-6273 ] ; 2016.
Abstract
Parkinson’s disease (PD) is a multifactorial neurodegenerative disorder, the etiology of which remains largely unknown. Progressive impairment of voluntary motor control, which represents the primary clinical feature of the disease, is caused by a loss of midbrain substantia nigra dopamine (DA) neurons. We present, here, a synthetic overview of cell autonomous mechanisms that are likely to participate in DA cell death in both sporadic and inherited forms of the disease. In particular, we describe how damage to vulnerable DA neurons may arise from cellular disturbances produced by protein misfolding and aggregation, disruption of autophagic catabolism, endoplasmic reticulum (ER) stress, mitochondrial dysfunction or loss of calcium homeostasis. Where pertinent, we show how these mechanisms may mutually cooperate to promote neuronal death.
Url:
DOI: 10.1016/j.neuron.2016.03.038
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<front><div type="abstract" xml:lang="en">Parkinson’s disease (PD) is a multifactorial neurodegenerative disorder, the etiology of which remains largely unknown. Progressive impairment of voluntary motor control, which represents the primary clinical feature of the disease, is caused by a loss of midbrain substantia nigra dopamine (DA) neurons. We present, here, a synthetic overview of cell autonomous mechanisms that are likely to participate in DA cell death in both sporadic and inherited forms of the disease. In particular, we describe how damage to vulnerable DA neurons may arise from cellular disturbances produced by protein misfolding and aggregation, disruption of autophagic catabolism, endoplasmic reticulum (ER) stress, mitochondrial dysfunction or loss of calcium homeostasis. Where pertinent, we show how these mechanisms may mutually cooperate to promote neuronal death.</div>
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<sourceDesc> <biblStruct> <analytic> <title xml:lang="en">Understanding Dopaminergic Cell Death Pathways in Parkinson Disease</title>
<title xml:lang="en" type="sub">Cell Death in Parkinson Disease</title>
<author role="aut"> <persName> <forename type="first">Stéphane</forename>
<surname>Hunot</surname>
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<idno type="halauthorid">527648</idno>
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<author role="crp"> <persName> <forename type="first">Etienne</forename>
<surname>Hirsch</surname>
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<author role="aut"> <persName> <forename type="first">Stéphane</forename>
<surname>Hunot</surname>
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<email type="md5">fa28ca54589b955ddde60eb30510aa8d</email>
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<title level="j">Neuron</title>
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<biblScope unit="pp">675-91</biblScope>
<date type="datePub">2016</date>
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<abstract xml:lang="en">Parkinson’s disease (PD) is a multifactorial neurodegenerative disorder, the etiology of which remains largely unknown. Progressive impairment of voluntary motor control, which represents the primary clinical feature of the disease, is caused by a loss of midbrain substantia nigra dopamine (DA) neurons. We present, here, a synthetic overview of cell autonomous mechanisms that are likely to participate in DA cell death in both sporadic and inherited forms of the disease. In particular, we describe how damage to vulnerable DA neurons may arise from cellular disturbances produced by protein misfolding and aggregation, disruption of autophagic catabolism, endoplasmic reticulum (ER) stress, mitochondrial dysfunction or loss of calcium homeostasis. Where pertinent, we show how these mechanisms may mutually cooperate to promote neuronal death.</abstract>
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