Parkinson's Disease, Cortical Dysfunction, and Alpha-Synuclein
Identifieur interne : 001A55 ( Main/Merge ); précédent : 001A54; suivant : 001A56Parkinson'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.
Descripteurs français
- Pascal (Inist)
English descriptors
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.
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Evidente</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurology, Mayo Clinic</s1><s2>Scottsdale, Arizona</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="05"><s1>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="05"><s1>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>États-Unis</country><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. 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Caviness</name><affiliation wicri:level="2"><inist:fA14 i1="01"><s1>Department of Neurology, Mayo Clinic</s1><s2>Scottsdale, Arizona</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Arizona</region></placeName></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"><inist:fA14 i1="02"><s1>Laboratory of Neuroinflammation, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="03"><s1>Civin Laboratory of Neuropathology, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="04"><s1>Department of Biostatistics, Mayo Clinic</s1><s2>Scottsdale, Arizona</s2><s3>USA</s3><sZ>4 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="01"><s1>Department of Neurology, Mayo Clinic</s1><s2>Scottsdale, Arizona</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="03"><s1>Civin Laboratory of Neuropathology, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="02"><s1>Laboratory of Neuroinflammation, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Arizona</region></placeName></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"><inist:fA14 i1="01"><s1>Department of Neurology, Mayo Clinic</s1><s2>Scottsdale, Arizona</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="01"><s1>Department of Neurology, Mayo Clinic</s1><s2>Scottsdale, Arizona</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>5 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="05"><s1>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="05"><s1>Cleo Roberts Clinical Research Center, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>10 aut.</sZ><sZ>11 aut.</sZ></inist:fA14><country>États-Unis</country><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"><inist:fA14 i1="02"><s1>Laboratory of Neuroinflammation, Banner Sun Health Research Institute</s1><s2>Sun City, Arizona</s2><s3>USA</s3><sZ>2 aut.</sZ><sZ>7 aut.</sZ><sZ>12 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Arizona</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Dementia</term><term>Dysfunction</term><term>Myoclonus</term><term>Nervous system diseases</term><term>Parkinson disease</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Myoclonie</term><term>Démence</term><term>Pathologie du système nerveux</term><term>Trouble fonctionnel</term></keywords></textClass></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.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Arizona</li></region></list><tree><country name="États-Unis"><region name="Arizona"><name sortKey="Caviness, John N" sort="Caviness, John N" uniqKey="Caviness J" first="John N." last="Caviness">John N. Caviness</name></region><name sortKey="Adler, Charles H" sort="Adler, Charles H" uniqKey="Adler C" first="Charles H." last="Adler">Charles H. Adler</name><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G." last="Beach">Thomas G. Beach</name><name sortKey="Driver Dunckley, Erika" sort="Driver Dunckley, Erika" uniqKey="Driver Dunckley E" first="Erika" last="Driver-Dunckley">Erika Driver-Dunckley</name><name sortKey="Evidente, Virgilio G" sort="Evidente, Virgilio G" uniqKey="Evidente V" first="Virgilio G." last="Evidente">Virgilio G. Evidente</name><name sortKey="Hentz, Joseph G" sort="Hentz, Joseph G" uniqKey="Hentz J" first="Joseph G." last="Hentz">Joseph G. Hentz</name><name sortKey="Lue, Lih Fen" sort="Lue, Lih Fen" uniqKey="Lue L" first="Lih-Fen" last="Lue">Lih-Fen Lue</name><name sortKey="Sabbagh, Marwan N" sort="Sabbagh, Marwan N" uniqKey="Sabbagh M" first="Marwan N." last="Sabbagh">Marwan N. Sabbagh</name><name sortKey="Sadeghi, Ramin" sort="Sadeghi, Ramin" uniqKey="Sadeghi R" first="Ramin" last="Sadeghi">Ramin Sadeghi</name><name sortKey="Shill, Holly A" sort="Shill, Holly A" uniqKey="Shill H" first="Holly A." last="Shill">Holly A. Shill</name><name sortKey="Sue, Lucia" sort="Sue, Lucia" uniqKey="Sue L" first="Lucia" last="Sue">Lucia Sue</name><name sortKey="Walker, Douglas G" sort="Walker, Douglas G" uniqKey="Walker D" first="Douglas G." last="Walker">Douglas G. Walker</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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