Milestones in Parkinson's disease--clinical and pathologic features.
Identifieur interne : 001176 ( PubMed/Corpus ); précédent : 001175; suivant : 001177Milestones in Parkinson's disease--clinical and pathologic features.
Auteurs : Glenda Halliday ; Andrew Lees ; Matthew SternSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Dopamine.
- complications : Parkinson Disease.
- history : Parkinson Disease.
- metabolism : Neurons.
- pathology : Lewy Bodies, Neurons, Parkinson Disease.
- therapy : Parkinson Disease.
- History, 20th Century, History, 21st Century, Humans.
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.
DOI: 10.1002/mds.23669
PubMed: 21626546
Links to Exploration step
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<author><name sortKey="Halliday, Glenda" sort="Halliday, Glenda" uniqKey="Halliday G" first="Glenda" last="Halliday">Glenda Halliday</name>
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<author><name sortKey="Lees, Andrew" sort="Lees, Andrew" uniqKey="Lees A" first="Andrew" last="Lees">Andrew Lees</name>
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<author><name sortKey="Stern, Matthew" sort="Stern, Matthew" uniqKey="Stern M" first="Matthew" last="Stern">Matthew Stern</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dopamine (metabolism)</term>
<term>History, 20th Century</term>
<term>History, 21st Century</term>
<term>Humans</term>
<term>Lewy Bodies (pathology)</term>
<term>Neurons (metabolism)</term>
<term>Neurons (pathology)</term>
<term>Parkinson Disease (complications)</term>
<term>Parkinson Disease (history)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (therapy)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term>
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<keywords scheme="MESH" qualifier="history" xml:lang="en"><term>Parkinson Disease</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term>
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<term>Neurons</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Parkinson Disease</term>
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<keywords scheme="MESH" xml:lang="en"><term>History, 20th Century</term>
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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.</div>
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<Abstract><AbstractText>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.</AbstractText>
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