Examining Braak's hypothesis by imaging Parkinson's disease
Identifieur interne : 001D01 ( Main/Exploration ); précédent : 001D00; suivant : 001D02Examining Braak's hypothesis by imaging Parkinson's disease
Auteurs : David J. Brooks [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Braak staging, Brain (blood supply), Brain (pathology), Brain (radionuclide imaging), Diagnostic Imaging (methods), Heart (innervation), Humans, Nervous system diseases, Neurotransmitter Agents (metabolism), Nuclear magnetic resonance imaging, Parkinson disease, Parkinson's disease, Parkinsonian Disorders (metabolism), Parkinsonian Disorders (pathology), Parkinsonian Disorders (radionuclide imaging), Photon, Positron emission tomography, Risk Factors, SPECT, Severity of Illness Index, Single photon emission tomography, Sonography, magnetic resonance imaging, positron emission tomography, transcranial sonography.
- MESH :
- chemical , metabolism : Neurotransmitter Agents.
- blood supply : Brain.
- innervation : Heart.
- metabolism : Parkinsonian Disorders.
- methods : Diagnostic Imaging.
- pathology : Brain, Parkinsonian Disorders.
- radionuclide imaging : Brain, Parkinsonian Disorders.
- Humans, Risk Factors, Severity of Illness Index.
Abstract
In this review, in vivo patterns of structural, metabolic, and neurotransmitter binding changes revealed by imaging in both symptomatic Parkinson's disease (PD) and at‐risk subjects are compared with those predicted at different Braak stages. It is concluded that the dysfunction revealed by imaging in PD is only partially in line with the sequential ascending topography of Lewy body pathology reported by Braak, suggesting that neurons in different brain regions are likely to be selectively vulnerable to the presence of intracellular synuclein aggregates. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.22720
Affiliations:
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Le document en format XML
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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="2010">2010</date><biblScope unit="vol">25</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="page" from="S83">S83</biblScope><biblScope unit="page" to="S88">S88</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9FC9CFC5E30A20A6F04A3E601E95AF16F2526928</idno><idno type="DOI">10.1002/mds.22720</idno><idno type="ArticleID">MDS22720</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Braak staging</term><term>Brain (blood supply)</term><term>Brain (pathology)</term><term>Brain (radionuclide imaging)</term><term>Diagnostic Imaging (methods)</term><term>Heart (innervation)</term><term>Humans</term><term>Nervous system diseases</term><term>Neurotransmitter Agents (metabolism)</term><term>Nuclear magnetic resonance imaging</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Parkinsonian Disorders (metabolism)</term><term>Parkinsonian Disorders (pathology)</term><term>Parkinsonian Disorders (radionuclide imaging)</term><term>Photon</term><term>Positron emission tomography</term><term>Risk Factors</term><term>SPECT</term><term>Severity of Illness Index</term><term>Single photon emission tomography</term><term>Sonography</term><term>magnetic resonance imaging</term><term>positron emission tomography</term><term>transcranial sonography</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Neurotransmitter Agents</term></keywords><keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="innervation" xml:lang="en"><term>Heart</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Diagnostic Imaging</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Brain</term><term>Parkinsonian Disorders</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term><term>Risk Factors</term><term>Severity of Illness Index</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Exploration ultrason</term><term>Imagerie RMN</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Photon</term><term>Tomographie par émission de positons</term><term>Tomoscintigraphie émission monophotonique</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In this review, in vivo patterns of structural, metabolic, and neurotransmitter binding changes revealed by imaging in both symptomatic Parkinson's disease (PD) and at‐risk subjects are compared with those predicted at different Braak stages. It is concluded that the dysfunction revealed by imaging in PD is only partially in line with the sequential ascending topography of Lewy body pathology reported by Braak, suggesting that neurons in different brain regions are likely to be selectively vulnerable to the presence of intracellular synuclein aggregates. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Brooks, David J" sort="Brooks, David J" uniqKey="Brooks D" first="David J." last="Brooks">David J. Brooks</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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