β-Amyloid and postural instability and gait difficulty in Parkinson's disease at risk for dementia.
Identifieur interne : 000B27 ( PubMed/Corpus ); précédent : 000B26; suivant : 000B28β-Amyloid and postural instability and gait difficulty in Parkinson's disease at risk for dementia.
Auteurs : Martijn L T M. Müller ; Kirk A. Frey ; Myria Petrou ; Vikas Kotagal ; Robert A. Koeppe ; Roger L. Albin ; Nicolaas I. BohnenSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2013.
English descriptors
- KwdEn :
- Aged, Aged, 80 and over, Amyloid beta-Peptides (metabolism), Aniline Compounds (diagnostic use), Carbon Isotopes (pharmacokinetics), Cross-Sectional Studies, Dementia (complications), Female, Gait Disorders, Neurologic (etiology), Humans, Magnetic Resonance Imaging, Male, Middle Aged, Parkinson Disease (complications), Parkinson Disease (metabolism), Parkinson Disease (radionuclide imaging), Positron-Emission Tomography, Postural Balance (physiology), Psychiatric Status Rating Scales, Sensation Disorders (etiology), Severity of Illness Index, Tetrabenazine (analogs & derivatives), Tetrabenazine (diagnostic use), Thiazoles (diagnostic use).
- MESH :
- chemical , analogs & derivatives : Tetrabenazine.
- chemical , diagnostic use : Aniline Compounds, Tetrabenazine, Thiazoles.
- chemical , metabolism : Amyloid beta-Peptides.
- chemical , pharmacokinetics : Carbon Isotopes.
- complications : Dementia, Parkinson Disease.
- etiology : Gait Disorders, Neurologic, Sensation Disorders.
- metabolism : Parkinson Disease.
- physiology : Postural Balance.
- radionuclide imaging : Parkinson Disease.
- Aged, Aged, 80 and over, Cross-Sectional Studies, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Positron-Emission Tomography, Psychiatric Status Rating Scales, Severity of Illness Index.
Abstract
Although motor impairments in Parkinson's disease (PD) are attributed to nigrostriatal dopaminergic denervation, postural instability and gait difficulty (PIGD) features are less responsive to dopaminergic medications. PIGD features are a risk factor also for the development of dementia in PD (PDD). These observations suggest that nondopaminergic mechanisms may contribute to axial motor impairments. The aim was to perform a correlative PET study to examine the relationship between neocortical β-amyloid deposition ([(11)C]-Pittsburgh Compound B), nigrostriatal dopaminergic denervation ([(11)C]-dihydrotetrabenazine), and PIGD feature severity in PD patients at risk for dementia. This was a cross-sectional study of 44 PD patients (11 female and 33 male; 69.5 ± 6.6 years of age; 7.0 ± 4.8 years motor disease duration; mean H & Y stage: 2.7 ± 0.5) who underwent PET, motor feature severity assessment using the Movement Disorder Society revised UPDRS, and the Dementia Rating Scale (DRS). Linear regression (R(2)(adj) = 0.147; F(4,39) = 2.85; P = 0.036) showed that increased PIGD feature severity was associated with increased neocortical [(11)C]-Pittsburgh Compound B binding (β = 0.346; t(39) = 2.13; P = 0.039) while controlling for striatal [(11)C]-dihydrotetrabenazine binding, age, and DRS total score. Increased neocortical β-amyloid deposition, even at low-range levels, is associated with higher PIGD feature severity in PD patients at risk for dementia. This finding may explain why the PIGD motor phenotype is a risk factor for the development of PDD.
DOI: 10.1002/mds.25213
PubMed: 23239424
Links to Exploration step
pubmed:23239424Le document en format XML
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Frey</name></author><author><name sortKey="Petrou, Myria" sort="Petrou, Myria" uniqKey="Petrou M" first="Myria" last="Petrou">Myria Petrou</name></author><author><name sortKey="Kotagal, Vikas" sort="Kotagal, Vikas" uniqKey="Kotagal V" first="Vikas" last="Kotagal">Vikas Kotagal</name></author><author><name sortKey="Koeppe, Robert A" sort="Koeppe, Robert A" uniqKey="Koeppe R" first="Robert A" last="Koeppe">Robert A. Koeppe</name></author><author><name sortKey="Albin, Roger L" sort="Albin, Roger L" uniqKey="Albin R" first="Roger L" last="Albin">Roger L. Albin</name></author><author><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I" last="Bohnen">Nicolaas I. 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Frey</name></author><author><name sortKey="Petrou, Myria" sort="Petrou, Myria" uniqKey="Petrou M" first="Myria" last="Petrou">Myria Petrou</name></author><author><name sortKey="Kotagal, Vikas" sort="Kotagal, Vikas" uniqKey="Kotagal V" first="Vikas" last="Kotagal">Vikas Kotagal</name></author><author><name sortKey="Koeppe, Robert A" sort="Koeppe, Robert A" uniqKey="Koeppe R" first="Robert A" last="Koeppe">Robert A. Koeppe</name></author><author><name sortKey="Albin, Roger L" sort="Albin, Roger L" uniqKey="Albin R" first="Roger L" last="Albin">Roger L. Albin</name></author><author><name sortKey="Bohnen, Nicolaas I" sort="Bohnen, Nicolaas I" uniqKey="Bohnen N" first="Nicolaas I" last="Bohnen">Nicolaas I. Bohnen</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2013" type="published">2013</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>Aniline Compounds (diagnostic use)</term><term>Carbon Isotopes (pharmacokinetics)</term><term>Cross-Sectional Studies</term><term>Dementia (complications)</term><term>Female</term><term>Gait Disorders, Neurologic (etiology)</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Parkinson Disease (complications)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (radionuclide imaging)</term><term>Positron-Emission Tomography</term><term>Postural Balance (physiology)</term><term>Psychiatric Status Rating Scales</term><term>Sensation Disorders (etiology)</term><term>Severity of Illness Index</term><term>Tetrabenazine (analogs & derivatives)</term><term>Tetrabenazine (diagnostic use)</term><term>Thiazoles (diagnostic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Tetrabenazine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="diagnostic use" xml:lang="en"><term>Aniline Compounds</term><term>Tetrabenazine</term><term>Thiazoles</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid beta-Peptides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Carbon Isotopes</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Dementia</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Gait Disorders, Neurologic</term><term>Sensation Disorders</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Postural Balance</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Aged, 80 and over</term><term>Cross-Sectional Studies</term><term>Female</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Male</term><term>Middle Aged</term><term>Positron-Emission Tomography</term><term>Psychiatric Status Rating Scales</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although motor impairments in Parkinson's disease (PD) are attributed to nigrostriatal dopaminergic denervation, postural instability and gait difficulty (PIGD) features are less responsive to dopaminergic medications. PIGD features are a risk factor also for the development of dementia in PD (PDD). These observations suggest that nondopaminergic mechanisms may contribute to axial motor impairments. The aim was to perform a correlative PET study to examine the relationship between neocortical β-amyloid deposition ([(11)C]-Pittsburgh Compound B), nigrostriatal dopaminergic denervation ([(11)C]-dihydrotetrabenazine), and PIGD feature severity in PD patients at risk for dementia. This was a cross-sectional study of 44 PD patients (11 female and 33 male; 69.5 ± 6.6 years of age; 7.0 ± 4.8 years motor disease duration; mean H & Y stage: 2.7 ± 0.5) who underwent PET, motor feature severity assessment using the Movement Disorder Society revised UPDRS, and the Dementia Rating Scale (DRS). Linear regression (R(2)(adj) = 0.147; F(4,39) = 2.85; P = 0.036) showed that increased PIGD feature severity was associated with increased neocortical [(11)C]-Pittsburgh Compound B binding (β = 0.346; t(39) = 2.13; P = 0.039) while controlling for striatal [(11)C]-dihydrotetrabenazine binding, age, and DRS total score. Increased neocortical β-amyloid deposition, even at low-range levels, is associated with higher PIGD feature severity in PD patients at risk for dementia. This finding may explain why the PIGD motor phenotype is a risk factor for the development of PDD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">23239424</PMID><DateCreated><Year>2013</Year><Month>03</Month><Day>25</Day></DateCreated><DateCompleted><Year>2013</Year><Month>09</Month><Day>20</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>04</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>28</Volume><Issue>3</Issue><PubDate><Year>2013</Year><Month>Mar</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>β-Amyloid and postural instability and gait difficulty in Parkinson's disease at risk for dementia.</ArticleTitle><Pagination><MedlinePgn>296-301</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.25213</ELocationID><Abstract><AbstractText>Although motor impairments in Parkinson's disease (PD) are attributed to nigrostriatal dopaminergic denervation, postural instability and gait difficulty (PIGD) features are less responsive to dopaminergic medications. PIGD features are a risk factor also for the development of dementia in PD (PDD). These observations suggest that nondopaminergic mechanisms may contribute to axial motor impairments. The aim was to perform a correlative PET study to examine the relationship between neocortical β-amyloid deposition ([(11)C]-Pittsburgh Compound B), nigrostriatal dopaminergic denervation ([(11)C]-dihydrotetrabenazine), and PIGD feature severity in PD patients at risk for dementia. This was a cross-sectional study of 44 PD patients (11 female and 33 male; 69.5 ± 6.6 years of age; 7.0 ± 4.8 years motor disease duration; mean H & Y stage: 2.7 ± 0.5) who underwent PET, motor feature severity assessment using the Movement Disorder Society revised UPDRS, and the Dementia Rating Scale (DRS). Linear regression (R(2)(adj) = 0.147; F(4,39) = 2.85; P = 0.036) showed that increased PIGD feature severity was associated with increased neocortical [(11)C]-Pittsburgh Compound B binding (β = 0.346; t(39) = 2.13; P = 0.039) while controlling for striatal [(11)C]-dihydrotetrabenazine binding, age, and DRS total score. Increased neocortical β-amyloid deposition, even at low-range levels, is associated with higher PIGD feature severity in PD patients at risk for dementia. This finding may explain why the PIGD motor phenotype is a risk factor for the development of PDD.</AbstractText><CopyrightInformation>Copyright © 2012 Movement Disorders Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Müller</LastName><ForeName>Martijn L T M</ForeName><Initials>ML</Initials><AffiliationInfo><Affiliation>Department of Radiology, University of Michigan, Ann Arbor, Michigan 48105, USA. mtmuller@med.umich.edu</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Frey</LastName><ForeName>Kirk A</ForeName><Initials>KA</Initials></Author><Author ValidYN="Y"><LastName>Petrou</LastName><ForeName>Myria</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Kotagal</LastName><ForeName>Vikas</ForeName><Initials>V</Initials></Author><Author ValidYN="Y"><LastName>Koeppe</LastName><ForeName>Robert A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Albin</LastName><ForeName>Roger L</ForeName><Initials>RL</Initials></Author><Author ValidYN="Y"><LastName>Bohnen</LastName><ForeName>Nicolaas I</ForeName><Initials>NI</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>P01 NS015655</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P50 NS015655</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS070856</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 NS070856</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType><PublicationType UI="D013486">Research Support, U.S. Gov't, Non-P.H.S.</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2012</Year><Month>12</Month><Day>12</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C475519">2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D016229">Amyloid beta-Peptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000814">Aniline Compounds</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002247">Carbon Isotopes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013844">Thiazoles</NameOfSubstance></Chemical><Chemical><RegistryNumber>3466-75-9</RegistryNumber><NameOfSubstance UI="C032811">dihydrotetrabenazine</NameOfSubstance></Chemical><Chemical><RegistryNumber>Z9O08YRN8O</RegistryNumber><NameOfSubstance UI="D013747">Tetrabenazine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>J Neurol Neurosurg Psychiatry. 2000 Sep;69(3):308-12</RefSource><PMID Version="1">10945804</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Mol Neurosci. 2002 Aug-Oct;19(1-2):11-6</RefSource><PMID Version="1">12212766</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Geriatr Psychiatry Neurol. 2003 Mar;16(1):53-8</RefSource><PMID Version="1">12641374</PMID></CommentsCorrections><CommentsCorrections 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