Parkinson's disease, cortical dysfunction, and alpha‐synuclein
Identifieur interne : 001539 ( Main/Merge ); précédent : 001538; suivant : 001540Parkinson's disease, cortical dysfunction, and alpha‐synuclein
Auteurs : John N. Caviness [États-Unis] ; Lih-Fen Lue [États-Unis] ; Thomas G. Beach [États-Unis] ; Joseph G. Hentz [États-Unis] ; Charles H. Adler [États-Unis] ; Lucia Sue [États-Unis] ; Ramin Sadeghi [États-Unis] ; Erika Driver-Dunckley [États-Unis] ; Virgilio G. Evidente [États-Unis] ; Marwan N. Sabbagh [États-Unis] ; Holly A. Shill [États-Unis] ; Douglas G. Walker [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-07.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Amyloid beta-Peptides (metabolism), Cerebral Cortex (physiopathology), Cognition Disorders (diagnosis), Cognition Disorders (etiology), Female, Humans, Male, Myoclonus (complications), Myoclonus (pathology), Nerve Tissue Proteins (metabolism), Neuropsychological Tests, Parkinson Disease (complications), Parkinson Disease (metabolism), Parkinson Disease (pathology), Parkinson's disease, Peptide Fragments (metabolism), alpha-Synuclein (metabolism), alpha‐synuclein, cortex, dementia, myoclonus.
- MESH :
- chemical , metabolism : Amyloid beta-Peptides, Nerve Tissue Proteins, Peptide Fragments, alpha-Synuclein.
- complications : Myoclonus, Parkinson Disease.
- diagnosis : Cognition Disorders.
- etiology : Cognition Disorders.
- metabolism : Parkinson Disease.
- pathology : Myoclonus, Parkinson Disease.
- physiopathology : Cerebral Cortex.
- Aged, Aged, 80 and over, Female, Humans, Male, Neuropsychological Tests.
Abstract
The ability to understand how Parkinson's disease neurodegeneration leads to cortical dysfunction will be critical for developing therapeutic advances in Parkinson's disease dementia. The overall purpose of this project was to study the small‐amplitude cortical myoclonus in Parkinson's disease as an in vivo model of focal cortical dysfunction secondary to Parkinson's disease neurodegeneration. The objectives were to test the hypothesis that cortical myoclonus in Parkinson's disease is linked to abnormal levels of α‐synuclein in the primary motor cortex and to define its relationship to various biochemical, clinical, and pathological measures. The primary motor cortex was evaluated for 11 Parkinson's disease subjects with and 8 without electrophysiologically confirmed cortical myoclonus (the Parkinson's disease + myoclonus group and the Parkinson's disease group, respectively) who had premortem movement and cognitive testing. Similarly assessed 9 controls were used for comparison. Measurements for α‐synuclein, Aβ‐42 peptide, and other biochemical measures were made in the primary motor cortex. A 36% increase in α‐synuclein was found in the motor cortex of Parkinson's disease + myoclonus cases when compared with Parkinson's disease without myoclonus. This occurred without significant differences in insoluble α‐synuclein, phosphorylated to total α‐synuclein ratio, or Aβ‐42 peptide levels. Higher total motor cortex α‐synuclein levels significantly correlated with the presence of cortical myoclonus but did not correlate with multiple clinical or pathological findings. These results suggest an association between elevated α‐synuclein and the dysfunctional physiology arising from the motor cortex in Parkinson's disease + myoclonus cases. Alzheimer's disease pathology was not associated with cortical myoclonus in Parkinson's disease. Cortical myoclonus arising from the motor cortex is a model to study cortical dysfunction in Parkinson's disease. © 2011 Movement Disorder Society
Url:
- https://api.istex.fr/document/144E863BBEAB2309251E849269B1DE105DB99D42/fulltext/pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154995
DOI: 10.1002/mds.23697
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ISTEX:144E863BBEAB2309251E849269B1DE105DB99D42Le document en format XML
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Shill</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Walker, Douglas G" sort="Walker, Douglas G" uniqKey="Walker D" first="Douglas G." last="Walker">Douglas G. Walker</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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="2011-07">2011-07</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1436">1436</biblScope><biblScope unit="page" to="1442">1442</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">144E863BBEAB2309251E849269B1DE105DB99D42</idno><idno type="DOI">10.1002/mds.23697</idno><idno type="ArticleID">MDS23697</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Amyloid beta-Peptides (metabolism)</term><term>Cerebral Cortex (physiopathology)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (etiology)</term><term>Female</term><term>Humans</term><term>Male</term><term>Myoclonus (complications)</term><term>Myoclonus (pathology)</term><term>Nerve Tissue Proteins (metabolism)</term><term>Neuropsychological Tests</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Parkinson's disease</term><term>Peptide Fragments (metabolism)</term><term>alpha-Synuclein (metabolism)</term><term>alpha‐synuclein</term><term>cortex</term><term>dementia</term><term>myoclonus</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid beta-Peptides</term><term>Nerve Tissue Proteins</term><term>Peptide Fragments</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Myoclonus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Myoclonus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The ability to understand how Parkinson's disease neurodegeneration leads to cortical dysfunction will be critical for developing therapeutic advances in Parkinson's disease dementia. The overall purpose of this project was to study the small‐amplitude cortical myoclonus in Parkinson's disease as an in vivo model of focal cortical dysfunction secondary to Parkinson's disease neurodegeneration. The objectives were to test the hypothesis that cortical myoclonus in Parkinson's disease is linked to abnormal levels of α‐synuclein in the primary motor cortex and to define its relationship to various biochemical, clinical, and pathological measures. The primary motor cortex was evaluated for 11 Parkinson's disease subjects with and 8 without electrophysiologically confirmed cortical myoclonus (the Parkinson's disease + myoclonus group and the Parkinson's disease group, respectively) who had premortem movement and cognitive testing. Similarly assessed 9 controls were used for comparison. Measurements for α‐synuclein, Aβ‐42 peptide, and other biochemical measures were made in the primary motor cortex. A 36% increase in α‐synuclein was found in the motor cortex of Parkinson's disease + myoclonus cases when compared with Parkinson's disease without myoclonus. This occurred without significant differences in insoluble α‐synuclein, phosphorylated to total α‐synuclein ratio, or Aβ‐42 peptide levels. Higher total motor cortex α‐synuclein levels significantly correlated with the presence of cortical myoclonus but did not correlate with multiple clinical or pathological findings. These results suggest an association between elevated α‐synuclein and the dysfunctional physiology arising from the motor cortex in Parkinson's disease + myoclonus cases. Alzheimer's disease pathology was not associated with cortical myoclonus in Parkinson's disease. Cortical myoclonus arising from the motor cortex is a model to study cortical dysfunction in Parkinson's disease. © 2011 Movement Disorder Society</div></front></TEI><double doi="10.1002/mds.23697"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Parkinson's disease, cortical dysfunction, and alpha‐synuclein</title><author><name sortKey="Caviness, John N" sort="Caviness, John N" uniqKey="Caviness J" first="John N." last="Caviness">John N. Caviness</name></author><author><name sortKey="Lue, Lih En" sort="Lue, Lih En" uniqKey="Lue L" first="Lih-Fen" last="Lue">Lih-Fen Lue</name></author><author><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G." last="Beach">Thomas G. Beach</name></author><author><name sortKey="Hentz, Joseph G" sort="Hentz, Joseph G" uniqKey="Hentz J" first="Joseph G." last="Hentz">Joseph G. Hentz</name></author><author><name sortKey="Adler, Charles H" sort="Adler, Charles H" uniqKey="Adler C" first="Charles H." last="Adler">Charles H. Adler</name></author><author><name sortKey="Sue, Lucia" sort="Sue, Lucia" uniqKey="Sue L" first="Lucia" last="Sue">Lucia Sue</name></author><author><name sortKey="Sadeghi, Ramin" sort="Sadeghi, Ramin" uniqKey="Sadeghi R" first="Ramin" last="Sadeghi">Ramin Sadeghi</name></author><author><name sortKey="Driver Unckley, Erika" sort="Driver Unckley, Erika" uniqKey="Driver Unckley E" first="Erika" last="Driver-Dunckley">Erika Driver-Dunckley</name></author><author><name sortKey="Evidente, Virgilio G" sort="Evidente, Virgilio G" uniqKey="Evidente V" first="Virgilio G." last="Evidente">Virgilio G. Evidente</name></author><author><name sortKey="Sabbagh, Marwan N" sort="Sabbagh, Marwan N" uniqKey="Sabbagh M" first="Marwan N." last="Sabbagh">Marwan N. Sabbagh</name></author><author><name sortKey="Shill, Holly A" sort="Shill, Holly A" uniqKey="Shill H" first="Holly A." last="Shill">Holly A. Shill</name></author><author><name sortKey="Walker, Douglas G" sort="Walker, Douglas G" uniqKey="Walker D" first="Douglas G." last="Walker">Douglas G. Walker</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:144E863BBEAB2309251E849269B1DE105DB99D42</idno><date when="2011" year="2011">2011</date><idno type="doi">10.1002/mds.23697</idno><idno type="url">https://api.istex.fr/document/144E863BBEAB2309251E849269B1DE105DB99D42/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">000441</idno><idno type="wicri:Area/Istex/Curation">000441</idno><idno type="wicri:Area/Istex/Checkpoint">000218</idno><idno type="wicri:doubleKey">0885-3185:2011:Caviness J:parkinson:s:disease</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Parkinson's disease, cortical dysfunction, and alpha‐synuclein</title><author><name sortKey="Caviness, John N" sort="Caviness, John N" uniqKey="Caviness J" first="John N." last="Caviness">John N. Caviness</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mayo Clinic, Scottsdale, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Lue, Lih En" sort="Lue, Lih En" uniqKey="Lue L" first="Lih-Fen" last="Lue">Lih-Fen Lue</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G." last="Beach">Thomas G. Beach</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Hentz, Joseph G" sort="Hentz, Joseph G" uniqKey="Hentz J" first="Joseph G." last="Hentz">Joseph G. Hentz</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Biostatistics, Mayo Clinic, Scottsdale, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Adler, Charles H" sort="Adler, Charles H" uniqKey="Adler C" first="Charles H." last="Adler">Charles H. Adler</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mayo Clinic, Scottsdale, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Sue, Lucia" sort="Sue, Lucia" uniqKey="Sue L" first="Lucia" last="Sue">Lucia Sue</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Sadeghi, Ramin" sort="Sadeghi, Ramin" uniqKey="Sadeghi R" first="Ramin" last="Sadeghi">Ramin Sadeghi</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Driver Unckley, Erika" sort="Driver Unckley, Erika" uniqKey="Driver Unckley E" first="Erika" last="Driver-Dunckley">Erika Driver-Dunckley</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mayo Clinic, Scottsdale, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Evidente, Virgilio G" sort="Evidente, Virgilio G" uniqKey="Evidente V" first="Virgilio G." last="Evidente">Virgilio G. Evidente</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mayo Clinic, Scottsdale, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Sabbagh, Marwan N" sort="Sabbagh, Marwan N" uniqKey="Sabbagh M" first="Marwan N." last="Sabbagh">Marwan N. Sabbagh</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Shill, Holly A" sort="Shill, Holly A" uniqKey="Shill H" first="Holly A." last="Shill">Holly A. Shill</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author><author><name sortKey="Walker, Douglas G" sort="Walker, Douglas G" uniqKey="Walker D" first="Douglas G." last="Walker">Douglas G. Walker</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Sun City, Arizona</wicri:regionArea><placeName><region type="state">Arizona</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="abbrev">Mov. 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="2011-07">2011-07</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">8</biblScope><biblScope unit="page" from="1436">1436</biblScope><biblScope unit="page" to="1442">1442</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">144E863BBEAB2309251E849269B1DE105DB99D42</idno><idno type="DOI">10.1002/mds.23697</idno><idno type="ArticleID">MDS23697</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>alpha‐synuclein</term><term>cortex</term><term>dementia</term><term>myoclonus</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The ability to understand how Parkinson's disease neurodegeneration leads to cortical dysfunction will be critical for developing therapeutic advances in Parkinson's disease dementia. The overall purpose of this project was to study the small‐amplitude cortical myoclonus in Parkinson's disease as an in vivo model of focal cortical dysfunction secondary to Parkinson's disease neurodegeneration. The objectives were to test the hypothesis that cortical myoclonus in Parkinson's disease is linked to abnormal levels of α‐synuclein in the primary motor cortex and to define its relationship to various biochemical, clinical, and pathological measures. The primary motor cortex was evaluated for 11 Parkinson's disease subjects with and 8 without electrophysiologically confirmed cortical myoclonus (the Parkinson's disease + myoclonus group and the Parkinson's disease group, respectively) who had premortem movement and cognitive testing. Similarly assessed 9 controls were used for comparison. Measurements for α‐synuclein, Aβ‐42 peptide, and other biochemical measures were made in the primary motor cortex. A 36% increase in α‐synuclein was found in the motor cortex of Parkinson's disease + myoclonus cases when compared with Parkinson's disease without myoclonus. This occurred without significant differences in insoluble α‐synuclein, phosphorylated to total α‐synuclein ratio, or Aβ‐42 peptide levels. Higher total motor cortex α‐synuclein levels significantly correlated with the presence of cortical myoclonus but did not correlate with multiple clinical or pathological findings. These results suggest an association between elevated α‐synuclein and the dysfunctional physiology arising from the motor cortex in Parkinson's disease + myoclonus cases. Alzheimer's disease pathology was not associated with cortical myoclonus in Parkinson's disease. Cortical myoclonus arising from the motor cortex is a model to study cortical dysfunction in Parkinson's disease. © 2011 Movement Disorder Society</div></front></TEI></ISTEX><PMC><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Parkinson’s Disease, Cortical Dysfunction, and Alpha-Synuclein</title><author><name sortKey="Caviness, John N" sort="Caviness, John N" uniqKey="Caviness J" first="John N." last="Caviness">John N. Caviness</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurology, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Neurology, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Lue, Lih Fen" sort="Lue, Lih Fen" uniqKey="Lue L" first="Lih-Fen" last="Lue">Lih-Fen Lue</name><affiliation wicri:level="2"><nlm:aff id="A2">Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G." last="Beach">Thomas G. Beach</name><affiliation wicri:level="2"><nlm:aff id="A3">Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Hentz, Joseph G" sort="Hentz, Joseph G" uniqKey="Hentz J" first="Joseph G." last="Hentz">Joseph G. Hentz</name><affiliation wicri:level="2"><nlm:aff id="A4">Department of Biostatistics, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Biostatistics, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Adler, Charles H" sort="Adler, Charles H" uniqKey="Adler C" first="Charles H." last="Adler">Charles H. Adler</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurology, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Neurology, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Sue, Lucia" sort="Sue, Lucia" uniqKey="Sue L" first="Lucia" last="Sue">Lucia Sue</name><affiliation wicri:level="2"><nlm:aff id="A3">Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Sadeghi, Ramin" sort="Sadeghi, Ramin" uniqKey="Sadeghi R" first="Ramin" last="Sadeghi">Ramin Sadeghi</name><affiliation wicri:level="2"><nlm:aff id="A2">Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Driver Dunckley, Erika" sort="Driver Dunckley, Erika" uniqKey="Driver Dunckley E" first="Erika" last="Driver-Dunckley">Erika Driver-Dunckley</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurology, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Neurology, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Evidente, Virgilio G" sort="Evidente, Virgilio G" uniqKey="Evidente V" first="Virgilio G." last="Evidente">Virgilio G. Evidente</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurology, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Neurology, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Sabbagh, Marwan N" sort="Sabbagh, Marwan N" uniqKey="Sabbagh M" first="Marwan N." last="Sabbagh">Marwan N. Sabbagh</name><affiliation wicri:level="2"><nlm:aff id="A5">Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City</wicri:cityArea></affiliation></author><author><name sortKey="Shill, Holly A" sort="Shill, Holly A" uniqKey="Shill H" first="Holly A." last="Shill">Holly A. Shill</name><affiliation wicri:level="2"><nlm:aff id="A5">Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City</wicri:cityArea></affiliation></author><author><name sortKey="Walker, Douglas G" sort="Walker, Douglas G" uniqKey="Walker D" first="Douglas G." last="Walker">Douglas G. Walker</name><affiliation wicri:level="2"><nlm:aff id="A2">Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">21542019</idno><idno type="pmc">3154995</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154995</idno><idno type="RBID">PMC:3154995</idno><idno type="doi">10.1002/mds.23697</idno><date when="2011">2011</date><idno type="wicri:Area/Pmc/Corpus">000142</idno><idno type="wicri:Area/Pmc/Curation">000142</idno><idno type="wicri:Area/Pmc/Checkpoint">000244</idno><idno type="wicri:source">PubMed</idno><idno type="wicri:Area/PubMed/Corpus">001222</idno><idno type="wicri:Area/PubMed/Curation">001222</idno><idno type="wicri:Area/PubMed/Checkpoint">001177</idno><idno type="wicri:Area/Ncbi/Merge">003205</idno><idno type="wicri:Area/Ncbi/Curation">003205</idno><idno type="wicri:Area/Ncbi/Checkpoint">003205</idno><idno type="wicri:doubleKey">0885-3185:2011:Caviness J:parkinson:s:disease</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Parkinson’s Disease, Cortical Dysfunction, and Alpha-Synuclein</title><author><name sortKey="Caviness, John N" sort="Caviness, John N" uniqKey="Caviness J" first="John N." last="Caviness">John N. Caviness</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurology, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Neurology, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Lue, Lih Fen" sort="Lue, Lih Fen" uniqKey="Lue L" first="Lih-Fen" last="Lue">Lih-Fen Lue</name><affiliation wicri:level="2"><nlm:aff id="A2">Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G." last="Beach">Thomas G. Beach</name><affiliation wicri:level="2"><nlm:aff id="A3">Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Hentz, Joseph G" sort="Hentz, Joseph G" uniqKey="Hentz J" first="Joseph G." last="Hentz">Joseph G. Hentz</name><affiliation wicri:level="2"><nlm:aff id="A4">Department of Biostatistics, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Biostatistics, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Adler, Charles H" sort="Adler, Charles H" uniqKey="Adler C" first="Charles H." last="Adler">Charles H. Adler</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurology, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Neurology, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Sue, Lucia" sort="Sue, Lucia" uniqKey="Sue L" first="Lucia" last="Sue">Lucia Sue</name><affiliation wicri:level="2"><nlm:aff id="A3">Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Civin Laboratory of Neuropathology, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Sadeghi, Ramin" sort="Sadeghi, Ramin" uniqKey="Sadeghi R" first="Ramin" last="Sadeghi">Ramin Sadeghi</name><affiliation wicri:level="2"><nlm:aff id="A2">Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Driver Dunckley, Erika" sort="Driver Dunckley, Erika" uniqKey="Driver Dunckley E" first="Erika" last="Driver-Dunckley">Erika Driver-Dunckley</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurology, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Neurology, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Evidente, Virgilio G" sort="Evidente, Virgilio G" uniqKey="Evidente V" first="Virgilio G." last="Evidente">Virgilio G. Evidente</name><affiliation wicri:level="2"><nlm:aff id="A1">Department of Neurology, Mayo Clinic, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Department of Neurology, Mayo Clinic, Scottsdale</wicri:cityArea></affiliation></author><author><name sortKey="Sabbagh, Marwan N" sort="Sabbagh, Marwan N" uniqKey="Sabbagh M" first="Marwan N." last="Sabbagh">Marwan N. Sabbagh</name><affiliation wicri:level="2"><nlm:aff id="A5">Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City</wicri:cityArea></affiliation></author><author><name sortKey="Shill, Holly A" sort="Shill, Holly A" uniqKey="Shill H" first="Holly A." last="Shill">Holly A. Shill</name><affiliation wicri:level="2"><nlm:aff id="A5">Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute, Sun City</wicri:cityArea></affiliation></author><author><name sortKey="Walker, Douglas G" sort="Walker, Douglas G" uniqKey="Walker D" first="Douglas G." last="Walker">Douglas G. Walker</name><affiliation wicri:level="2"><nlm:aff id="A2">Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale, Arizona</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Arizona</region></placeName><wicri:cityArea>Laboratory of Neuroinflammation, Banner Sun Health Research Institute, Scottsdale</wicri:cityArea></affiliation></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Amyloid beta-Peptides (metabolism)</term><term>Cerebral Cortex (physiopathology)</term><term>Cognition Disorders (diagnosis)</term><term>Cognition Disorders (etiology)</term><term>Female</term><term>Humans</term><term>Male</term><term>Myoclonus (complications)</term><term>Myoclonus (pathology)</term><term>Nerve Tissue Proteins (metabolism)</term><term>Neuropsychological Tests</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Peptide Fragments (metabolism)</term><term>alpha-Synuclein (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid beta-Peptides</term><term>Nerve Tissue Proteins</term><term>Peptide Fragments</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Myoclonus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Myoclonus</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Cerebral Cortex</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Female</term><term>Humans</term><term>Male</term><term>Neuropsychological Tests</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title><p id="P1">The ability to understand how Parkinson’s disease (PD) neurodegeneration leads to cortical dysfunction will be critical for developing therapeutic advances in PD dementia (PD-D). The overall purpose of this project was to study the small amplitude cortical myoclonus in PD as an <italic>in vivo</italic> model of focal cortical dysfunction secondary to PD neurodegeneration. The objectives were to test the hypothesis that cortical myoclonus in PD is linked to abnormal levels of α-synuclein in primary motor cortex and to define its relationship to various biochemical, clinical, and pathological measures.</p></sec><sec sec-type="methods" id="S2"><title>Methods</title><p id="P2">Primary motor cortex was evaluated for 11 PD subjects with (PD+Myoclonus group) and 8 without (PD group) electrophysiologically confirmed cortical myoclonus who had premortem movement and cognitive testing. Similarly assessed 9 controls were used for comparison. Measurements for α-synuclein, Aβ-42 peptide, and other biochemical measures were made in primary motor cortex.</p></sec><sec id="S3"><title>Results</title><p id="P3">A 36% increase in α-synuclein was found in the motor cortex of PD+Myoclonus cases when compared to PD without myoclonus. This occurred without significant differences in insoluble α-synuclein, phosphorylated to total α-synuclein ratio, or Aβ-42 peptide levels. Higher total motor cortex α-synuclein levels significantly correlated with the presence of cortical myoclonus but did not correlate with multiple clinical or pathological findings.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">These results suggest an association between elevated α-synuclein and the dysfunctional physiology arising from the motor cortex in PD+Myoclonus cases. Alzheimer’s disease pathology was not associated with cortical myoclonus in PD. Cortical myoclonus arising from motor cortex is a model to study cortical dysfunction in PD.</p></sec></div></front></TEI></PMC></double></record>Pour manipuler ce document sous Unix (Dilib)
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