Clues to how alpha‐synuclein damages neurons in Parkinson's disease
Identifieur interne : 001D87 ( Main/Exploration ); précédent : 001D86; suivant : 001D88Clues to how alpha‐synuclein damages neurons in Parkinson's disease
Auteurs : David Sulzer [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Humans, Inflammation (etiology), Lipids, Mutation (genetics), Nervous system diseases, Neuron, Neurons (cytology), Neurons (metabolism), Parkinson Disease (complications), Parkinson Disease (etiology), Parkinson Disease (genetics), Parkinson Disease (pathology), Parkinson disease, Parkinson's disease, Secretory Vesicles (genetics), Secretory Vesicles (metabolism), Secretory Vesicles (pathology), alpha-Synuclein (genetics), alpha-Synuclein (metabolism), alpha‐synuclein.
- MESH :
- chemical , genetics : alpha-Synuclein.
- chemical , metabolism : alpha-Synuclein.
- chemical : Lipids.
- complications : Parkinson Disease.
- cytology : Neurons.
- etiology : Inflammation, Parkinson Disease.
- genetics : Mutation, Parkinson Disease, Secretory Vesicles.
- metabolism : Neurons, Secretory Vesicles.
- pathology : Parkinson Disease, Secretory Vesicles.
- Humans.
Abstract
Alpha‐synuclein (α‐syn) appears to normally regulate neurotransmitter release, possibly via calcium‐dependent binding and dissociation from lipid domains on secretory vesicles. The pathogenic effects of α‐syn leading to Parkinson's disease (PD) appear to result from alternate toxic effects on lipid membrane. A variety of findings indicate that overexpression of wild‐type α‐syn, pathogenic mutations of α‐syn, and dopamine‐modified‐α‐syn promote toxic interaction between α‐syn oligomers and lipids. These may disrupt transmembrane concentration gradients across secretory vesicles and other organelles and interfere with normal lysosomal or ubiqutin/proteasome mediated protein degradation or mitochondrial function. Additional causes of PD may interfere at other points with normal handling and degradation of α‐syn, providing a variety of entry points to a converging neurodegenerative path underlying the disease. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.22639
Affiliations:
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Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2010">2010</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="page" from="S27">S27</biblScope><biblScope unit="page" to="S31">S31</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">CCFB2EFCF493516B40014F6EC820F194F9DB33FE</idno><idno type="DOI">10.1002/mds.22639</idno><idno type="ArticleID">MDS22639</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Humans</term><term>Inflammation (etiology)</term><term>Lipids</term><term>Mutation (genetics)</term><term>Nervous system diseases</term><term>Neuron</term><term>Neurons (cytology)</term><term>Neurons (metabolism)</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (etiology)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Secretory Vesicles (genetics)</term><term>Secretory Vesicles (metabolism)</term><term>Secretory Vesicles (pathology)</term><term>alpha-Synuclein (genetics)</term><term>alpha-Synuclein (metabolism)</term><term>alpha‐synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" type="chemical" xml:lang="en"><term>Lipids</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Inflammation</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mutation</term><term>Parkinson Disease</term><term>Secretory Vesicles</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term><term>Secretory Vesicles</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Secretory Vesicles</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Neurone</term><term>Pathologie du système nerveux</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Alpha‐synuclein (α‐syn) appears to normally regulate neurotransmitter release, possibly via calcium‐dependent binding and dissociation from lipid domains on secretory vesicles. The pathogenic effects of α‐syn leading to Parkinson's disease (PD) appear to result from alternate toxic effects on lipid membrane. A variety of findings indicate that overexpression of wild‐type α‐syn, pathogenic mutations of α‐syn, and dopamine‐modified‐α‐syn promote toxic interaction between α‐syn oligomers and lipids. These may disrupt transmembrane concentration gradients across secretory vesicles and other organelles and interfere with normal lysosomal or ubiqutin/proteasome mediated protein degradation or mitochondrial function. Additional causes of PD may interfere at other points with normal handling and degradation of α‐syn, providing a variety of entry points to a converging neurodegenerative path underlying the disease. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><country name="États-Unis"><region name="État de New York"><name sortKey="Sulzer, David" sort="Sulzer, David" uniqKey="Sulzer D" first="David" last="Sulzer">David Sulzer</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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