Milestones in Parkinson's disease—Clinical and pathologic features
Identifieur interne : 000565 ( Istex/Corpus ); précédent : 000564; suivant : 000566Milestones in Parkinson's disease—Clinical and pathologic features
Auteurs : Glenda Halliday ; Andrew Lees ; Matthew SternSource :
- Movement Disorders [ 0885-3185 ] ; 2011-05.
English descriptors
Abstract
The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society
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DOI: 10.1002/mds.23669
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<front><div type="abstract" xml:lang="en">The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society</div>
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<notesStmt><note type="content">*Relevant conflicts of interest/financial disclosures: Glenda Halliday is a Senior Principal Research Fellowship of the National Health and Medical Research Council of Australia (fellowship #350827). Andrew Lees receives funding from the Weston Trust and the PSP (Europe) Association. Matthew Stern is a consultant to Teva, Medtronic, Ipsen, Schering‐Plough, Adamas, and Novartis.Full financial disclosures and author roles may be found in the online version of this article.</note>
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<p>The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society</p>
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<abstract lang="en">The identification of the widespread deposition of fibrillized α‐synuclein in Lewy bodies and Lewy neurites in the brains of patients with Parkinson's disease in 1997 has had a profound impact on how the disease is now conceptualized. The previous focus on the loss of the dopaminergic nigrostriatal system, the concept of subcortical dementia, and the idea that Parkinson's disease was dominated by motor impairment have all given way to research assessing more diverse brain regions, clinical symptoms, and phenotypes. It is now recognized that Parkinson's disease is more than just a loss of midbrain dopaminergic neurons in association with Lewy bodies. There are now several theories on how the disease develops and progresses currently being validated in a variety of studies, although many of these theories have yet to incorporate the phenotypic clinical and pathological changes associated with age. A particularly exciting new area of research involves the cell‐to‐cell transmission of pathogenic proteins. The recent consensus definition of Parkinson's disease dementia will allow its pathologic substrates to be determined. These advances have progressed to a stage where the preclinical stages of Parkinson's disease and its specific signs and symptoms are being predicted and tested clinically. Such strategies herald a future wave of preventive strategies for Parkinson's disease and its clinical symptoms. © 2011 Movement Disorder Society</abstract>
<note type="content">*Relevant conflicts of interest/financial disclosures: Glenda Halliday is a Senior Principal Research Fellowship of the National Health and Medical Research Council of Australia (fellowship #350827). Andrew Lees receives funding from the Weston Trust and the PSP (Europe) Association. Matthew Stern is a consultant to Teva, Medtronic, Ipsen, Schering‐Plough, Adamas, and Novartis. Full financial disclosures and author roles may be found in the online version of this article.</note>
<subject lang="en"><genre>Keywords</genre>
<topic>α‐synuclein</topic>
<topic>Lewy bodies</topic>
<topic>neuropathology</topic>
<topic>preclinical Parkinson's disease</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Movement Disorders</title>
</titleInfo>
<titleInfo type="abbreviated"><title>Mov. Disord.</title>
</titleInfo>
<subject><genre>article category</genre>
<topic>Review</topic>
</subject>
<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>2011</date>
<detail type="title"><title>25th Anniversary</title>
</detail>
<detail type="volume"><caption>vol.</caption>
<number>26</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>6</number>
</detail>
<extent unit="pages"><start>1015</start>
<end>1021</end>
<total>7</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">D3143478950ED27D311D670FCE4BA2216869276B</identifier>
<identifier type="DOI">10.1002/mds.23669</identifier>
<identifier type="ArticleID">MDS23669</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition>
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<recordContentSource>WILEY</recordContentSource>
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