Recessive Parkinson's disease
Identifieur interne : 001216 ( Istex/Corpus ); précédent : 001215; suivant : 001217Recessive Parkinson's disease
Auteurs : Shin-Ichiro Kubo ; Nobutaka Hattori ; Yoshikuni MizunoSource :
- Movement Disorders [ 0885-3185 ] ; 2006-07.
English descriptors
- KwdEn :
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
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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, PINK1, and DJ‐1. © 2006 Movement Disorder Society</div>
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<p>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 <i>parkin</i>
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<abstract 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</abstract>
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<topic>ubiquitin–proteasome system</topic>
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<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
<subTitle>Official Journal of the Movement Disorder Society</subTitle>
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<titleInfo type="abbreviated"><title>Mov. Disord.</title>
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<subject><genre>article category</genre>
<topic>Research Review</topic>
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<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part><date>2006</date>
<detail type="volume"><caption>vol.</caption>
<number>21</number>
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<detail type="issue"><caption>no.</caption>
<number>7</number>
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<extent unit="pages"><start>885</start>
<end>893</end>
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<identifier type="istex">11A1C677F7100DB04F91F2EF9CE3CBB879261529</identifier>
<identifier type="DOI">10.1002/mds.20841</identifier>
<identifier type="ArticleID">MDS20841</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Movement Disorder Society</accessCondition>
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<recordContentSource>WILEY</recordContentSource>
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