Recessive Parkinson's disease
Identifieur interne : 003221 ( Main/Curation ); précédent : 003220; suivant : 003222Recessive Parkinson's disease
Auteurs : Shin-Ichiro Kubo [Japon] ; Nobutaka Hattori [Japon] ; Yoshikuni Mizuno [Japon]Source :
- Movement Disorders [ 0885-3185 ] ; 2006-07.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- DJ‐1, Dopamine (metabolism), Humans, Intracellular Signaling Peptides and Proteins (genetics), Mitochondria, Mitochondria (genetics), Mitochondria (physiology), Multicatalytic endopeptidase complex, Nervous system diseases, Oncogene Proteins (genetics), Oxidative Stress (genetics), Oxidative Stress (physiology), Oxidative stress, PINK1, Parkin, Parkinson disease, Parkinsonian Disorders (diagnosis), Parkinsonian Disorders (genetics), Parkinsonian Disorders (physiopathology), Phenotype, Proteasome Endopeptidase Complex (genetics), Proteasome Endopeptidase Complex (physiology), Protein Kinases (genetics), Substantia Nigra (physiopathology), Ubiquitin, Ubiquitin (genetics), Ubiquitin (metabolism), Ubiquitin-Protein Ligases (genetics), mitochondria, oxidative stress, parkin, recessive Parkinson's disease, ubiquitin–proteasome system.
- MESH :
- chemical , genetics : Intracellular Signaling Peptides and Proteins, Oncogene Proteins, Proteasome Endopeptidase Complex, Protein Kinases, Ubiquitin, Ubiquitin-Protein Ligases.
- chemical , metabolism : Dopamine, Ubiquitin.
- diagnosis : Parkinsonian Disorders.
- genetics : Mitochondria, Oxidative Stress, Parkinsonian Disorders.
- physiology : Mitochondria, Oxidative Stress, Proteasome Endopeptidase Complex.
- physiopathology : Parkinsonian Disorders, Substantia Nigra.
- Humans, Phenotype.
Abstract
Parkinson's disease (PD) is a progressive neurodegenerative disease caused by loss of dopaminergic neurons in the substantia nigra pars compacta. Although the etiology of PD remains unclear, it is now clear that genetic factors contribute to the pathogenesis of the disease. Recently, several causative genes have been identified in monogenic forms of PD. Accumulating evidence indicates that their gene products play important roles in mitochondrial function, oxidative stress response, and the ubiquitin–proteasome system, which are also implicated in sporadic PD, suggesting that these gene products share a common pathway to nigral degeneration in both familial and sporadic PD. Here, we review recent advances in knowledge about genes associated with recessive PD, including parkin, PINK1, and DJ‐1. © 2006 Movement Disorder Society
Url:
DOI: 10.1002/mds.20841
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<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a progressive neurodegenerative disease caused by loss of dopaminergic neurons in the substantia nigra pars compacta. Although the etiology of PD remains unclear, it is now clear that genetic factors contribute to the pathogenesis of the disease. Recently, several causative genes have been identified in monogenic forms of PD. Accumulating evidence indicates that their gene products play important roles in mitochondrial function, oxidative stress response, and the ubiquitin-proteasome system, which are also implicated in sporadic PD, suggesting that these gene products share a common pathway to nigral degeneration in both familial and sporadic PD. Here, we review recent advances in knowledge about genes associated with recessive PD, including parkin, PINKI, and DJ-1.</div>
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</author>
<author><name sortKey="Hattori, Nobutaka" sort="Hattori, Nobutaka" uniqKey="Hattori N" first="Nobutaka" last="Hattori">Nobutaka Hattori</name>
<affiliation wicri:level="3"><country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Neurology, Juntendo University School of Medicine, Tokyo</wicri:regionArea>
<placeName><settlement type="city">Tokyo</settlement>
</placeName>
</affiliation>
<affiliation wicri:level="3"><country xml:lang="fr">Japon</country>
<wicri:regionArea>Research Institute for Diseases of Old Age, Juntendo University School of Medicine, Tokyo</wicri:regionArea>
<placeName><settlement type="city">Tokyo</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Mizuno, Yoshikuni" sort="Mizuno, Yoshikuni" uniqKey="Mizuno Y" first="Yoshikuni" last="Mizuno">Yoshikuni Mizuno</name>
<affiliation wicri:level="3"><country xml:lang="fr">Japon</country>
<wicri:regionArea>Department of Neurology, Juntendo University School of Medicine, Tokyo</wicri:regionArea>
<placeName><settlement type="city">Tokyo</settlement>
</placeName>
</affiliation>
<affiliation wicri:level="3"><country xml:lang="fr">Japon</country>
<wicri:regionArea>Research Institute for Diseases of Old Age, Juntendo University School of Medicine, Tokyo</wicri:regionArea>
<placeName><settlement type="city">Tokyo</settlement>
</placeName>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series><title level="j">Movement Disorders</title>
<title level="j" type="sub">Official Journal of the Movement Disorder Society</title>
<title level="j" type="abbrev">Mov. 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="2006-07">2006-07</date>
<biblScope unit="vol">21</biblScope>
<biblScope unit="issue">7</biblScope>
<biblScope unit="page" from="885">885</biblScope>
<biblScope unit="page" to="893">893</biblScope>
</imprint>
<idno type="ISSN">0885-3185</idno>
</series>
<idno type="istex">11A1C677F7100DB04F91F2EF9CE3CBB879261529</idno>
<idno type="DOI">10.1002/mds.20841</idno>
<idno type="ArticleID">MDS20841</idno>
</biblStruct>
</sourceDesc>
<seriesStmt><idno type="ISSN">0885-3185</idno>
</seriesStmt>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>DJ‐1</term>
<term>Dopamine (metabolism)</term>
<term>Humans</term>
<term>Intracellular Signaling Peptides and Proteins (genetics)</term>
<term>Mitochondria (genetics)</term>
<term>Mitochondria (physiology)</term>
<term>Oncogene Proteins (genetics)</term>
<term>Oxidative Stress (genetics)</term>
<term>Oxidative Stress (physiology)</term>
<term>PINK1</term>
<term>Parkinsonian Disorders (diagnosis)</term>
<term>Parkinsonian Disorders (genetics)</term>
<term>Parkinsonian Disorders (physiopathology)</term>
<term>Phenotype</term>
<term>Proteasome Endopeptidase Complex (genetics)</term>
<term>Proteasome Endopeptidase Complex (physiology)</term>
<term>Protein Kinases (genetics)</term>
<term>Substantia Nigra (physiopathology)</term>
<term>Ubiquitin (genetics)</term>
<term>Ubiquitin (metabolism)</term>
<term>Ubiquitin-Protein Ligases (genetics)</term>
<term>mitochondria</term>
<term>oxidative stress</term>
<term>parkin</term>
<term>recessive Parkinson's disease</term>
<term>ubiquitin–proteasome system</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Intracellular Signaling Peptides and Proteins</term>
<term>Oncogene Proteins</term>
<term>Proteasome Endopeptidase Complex</term>
<term>Protein Kinases</term>
<term>Ubiquitin</term>
<term>Ubiquitin-Protein Ligases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term>
<term>Ubiquitin</term>
</keywords>
<keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinsonian Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Mitochondria</term>
<term>Oxidative Stress</term>
<term>Parkinsonian Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Mitochondria</term>
<term>Oxidative Stress</term>
<term>Proteasome Endopeptidase Complex</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinsonian Disorders</term>
<term>Substantia Nigra</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Humans</term>
<term>Phenotype</term>
</keywords>
</textClass>
<langUsage><language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a progressive neurodegenerative disease caused by loss of dopaminergic neurons in the substantia nigra pars compacta. Although the etiology of PD remains unclear, it is now clear that genetic factors contribute to the pathogenesis of the disease. Recently, several causative genes have been identified in monogenic forms of PD. Accumulating evidence indicates that their gene products play important roles in mitochondrial function, oxidative stress response, and the ubiquitin–proteasome system, which are also implicated in sporadic PD, suggesting that these gene products share a common pathway to nigral degeneration in both familial and sporadic PD. Here, we review recent advances in knowledge about genes associated with recessive PD, including parkin, PINK1, and DJ‐1. © 2006 Movement Disorder Society</div>
</front>
</TEI>
</ISTEX>
</double>
</record>
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