Detrimental deletions: mitochondria, aging and Parkinson's disease
Identifieur interne : 002E50 ( Main/Corpus ); précédent : 002E49; suivant : 002E51Detrimental deletions: mitochondria, aging and Parkinson's disease
Auteurs : Saskia Biskup ; Darren J. MooreSource :
- BioEssays [ 0265-9247 ] ; 2006-10.
Abstract
As individuals enter their 80s, they are inevitably confronted with the problem of neuronal loss in the brain. The incidence of the common movement disorder ‘mild parkinsonian signs’ (MPS) is approximately 50% over the age of 85 years. It has long been known that the loss of dopaminergic neurons in the substantia nigra pars compacta is a neuropathological hallmark of Parkinson's disease (PD). Recently, two papers1,2 present clear evidence for a high burden of mitochondrial DNA deletions within substantia nigra neurons in aged individuals and individuals with PD, pointing towards a common pathway inevitably leading to neuronal dysfunction and death. BioEssays 28: 963–967, 2006. © 2006 Wiley Periodicals, Inc.
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DOI: 10.1002/bies.20471
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The incidence of the common movement disorder ‘mild parkinsonian signs’ (MPS) is approximately 50% over the age of 85 years. It has long been known that the loss of dopaminergic neurons in the substantia nigra pars compacta is a neuropathological hallmark of Parkinson's disease (PD). Recently, two papers1,2 present clear evidence for a high burden of mitochondrial DNA deletions within substantia nigra neurons in aged individuals and individuals with PD, pointing towards a common pathway inevitably leading to neuronal dysfunction and death. 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The incidence of the common movement disorder ‘mild parkinsonian signs’ (MPS) is approximately 50% over the age of 85 years. It has long been known that the loss of dopaminergic neurons in the substantia nigra pars compacta is a neuropathological hallmark of Parkinson's disease (PD). Recently, two papers1,2 present clear evidence for a high burden of mitochondrial DNA deletions within substantia nigra neurons in aged individuals and individuals with PD, pointing towards a common pathway inevitably leading to neuronal dysfunction and death. BioEssays 28: 963–967, 2006. © 2006 Wiley Periodicals, Inc.</abstract><note type="funding">NIH/NINDS</note><note type="funding">National Parkinson Foundation</note><note type="funding">Michael J. Fox Foundation for Parkinson's Research</note><note type="funding">American Parkinson Disease Association</note><note type="funding">German Research Foundation (Deutsche Forschungsgemeinschaft)</note><relatedItem type="host"><titleInfo><title>BioEssays</title></titleInfo><titleInfo type="abbreviated"><title>Bioessays</title></titleInfo><genre type="Journal">journal</genre><subject><genre>article category</genre><topic>What the papers say</topic></subject><identifier type="ISSN">0265-9247</identifier><identifier type="eISSN">1521-1878</identifier><identifier type="DOI">10.1002/(ISSN)1521-1878</identifier><identifier type="PublisherID">BIES</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>28</number></detail><detail type="issue"><caption>no.</caption><number>10</number></detail><extent unit="pages"><start>963</start><end>967</end><total>5</total></extent></part></relatedItem><identifier type="istex">E1B714F29AF3653C720CE13483687B581007197E</identifier><identifier type="DOI">10.1002/bies.20471</identifier><identifier type="ArticleID">BIES20471</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2006 Wiley Periodicals, Inc.</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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