ParkinsonFranceV1, Hal, Curation, bibRecord, 000A73

Understanding Dopaminergic Cell Death Pathways in Parkinson Disease

Identifieur interne : 000A73 ( Hal/Curation ); précédent : 000A72; suivant : 000A74

Understanding Dopaminergic Cell Death Pathways in Parkinson Disease

Auteurs : Stéphane Hunot [France] ; Etienne Hirsch [France] ; Stéphane Hunot [France]

Source :

Neuron [ 0896-6273 ] ; 2016.

RBID : Hal:inserm-01348875

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:

http://www.hal.inserm.fr/inserm-01348875

DOI: 10.1016/j.neuron.2016.03.038

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Le document en format XML

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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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            <idno type="stamp" n="UPMC">Université Pierre et Marie Curie</idno>
            <idno type="stamp" n="ICM" p="UPMC">Institut du Cerveau et de la Moëlle Epinière</idno>
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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>
                  </persName>
                  <idno type="halauthorid">527648</idno>
                  <affiliation ref="#struct-246044"></affiliation>
                </author>
                <author role="crp">                  <persName>                    <forename type="first">Etienne</forename>
                    <surname>Hirsch</surname>
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                  <email type="md5">96464aee82d9a8c8cb07ffcdce3abe7f</email>
                  <email type="domain">upmc.fr</email>
                  <idno type="halauthorid">873083</idno>
                  <affiliation ref="#struct-246044"></affiliation>
                </author>
                <author role="aut">                  <persName>                    <forename type="first">Stéphane</forename>
                    <surname>Hunot</surname>
                  </persName>
                  <email type="md5">fa28ca54589b955ddde60eb30510aa8d</email>
                  <email type="domain">upmc.fr</email>
                  <idno type="halauthorid">412021</idno>
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                <title level="j">Neuron</title>
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                  <biblScope unit="volume">90</biblScope>
                  <biblScope unit="issue">(4)</biblScope>
                  <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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	La maladie de Parkinson en France (serveur d'exploration)
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La maladie de Parkinson en France (serveur d'exploration)

Understanding Dopaminergic Cell Death Pathways in Parkinson Disease

Understanding Dopaminergic Cell Death Pathways in Parkinson Disease

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