MovDisordV3, Ncbi, Curation, bibRecord, 003205

Parkinson’s Disease, Cortical Dysfunction, and Alpha-Synuclein

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Parkinson’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 : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2011.

RBID : PMC:3154995

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), Peptide Fragments (metabolism), alpha-Synuclein (metabolism).
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

Background

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 in vivo 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.

Methods

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.

Results

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.

Conclusions

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.

Url:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3154995

DOI: 10.1002/mds.23697
PubMed: 21542019
PubMed Central: 3154995

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PMC:3154995

Le document en format XML

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<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>
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<author><name sortKey="Lue, Lih Fen" sort="Lue, Lih Fen" uniqKey="Lue L" first="Lih-Fen" last="Lue">Lih-Fen Lue</name>
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<author><name sortKey="Beach, Thomas G" sort="Beach, Thomas G" uniqKey="Beach T" first="Thomas G." last="Beach">Thomas G. Beach</name>
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<author><name sortKey="Sabbagh, Marwan N" sort="Sabbagh, Marwan N" uniqKey="Sabbagh M" first="Marwan N." last="Sabbagh">Marwan N. Sabbagh</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Arizona</region>
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<wicri:cityArea>Department of Biostatistics, Mayo Clinic, Scottsdale</wicri:cityArea>
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<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>
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<author><name sortKey="Sue, Lucia" sort="Sue, Lucia" uniqKey="Sue L" first="Lucia" last="Sue">Lucia Sue</name>
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<country xml:lang="fr">États-Unis</country>
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<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>
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<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>
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<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>
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<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>
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<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>
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<author><name sortKey="Walker, Douglas G" sort="Walker, Douglas G" uniqKey="Walker D" first="Douglas G." last="Walker">Douglas G. Walker</name>
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<country xml:lang="fr">États-Unis</country>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<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>
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<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>
</record>

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	Movement Disorders (revue)
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Movement Disorders (revue)

Parkinson’s Disease, Cortical Dysfunction, and Alpha-Synuclein

Parkinson’s Disease, Cortical Dysfunction, and Alpha-Synuclein

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English descriptors

Abstract

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