Amyloid imaging of Lewy body‐associated disorders
Identifieur interne : 000820 ( Main/Exploration ); précédent : 000819; suivant : 000821Amyloid imaging of Lewy body‐associated disorders
Auteurs : Erin R. Foster [États-Unis] ; Meghan C. Campbell [États-Unis] ; Michelle A. Burack [États-Unis] ; Johanna Hartlein [États-Unis] ; Hubert P. Flores [États-Unis] ; Nigel J. Cairns [États-Unis] ; Tamara Hershey [États-Unis] ; Joel S. Perlmutter [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2010-11-15.
English descriptors
Abstract
Clinicopathologic studies of Parkinson disease dementia (PDD) and dementia with Lewy bodies (DLB) commonly reveal abnormal β‐amyloid deposition in addition to diffuse Lewy bodies (α‐synuclein aggregates), but the relationship among these neuropathologic features and the development of dementia in these disorders remains uncertain. The purpose of this study was to determine whether amyloid‐β deposition detected by PET imaging with Pittsburgh Compound B (PIB) distinguishes clinical subtypes of Lewy body‐associated disorders. Nine healthy controls, 8 PD with no cognitive impairment, 9 PD with mild cognitive impairment, 6 DLB, and 15 PDD patients underwent [11C]‐PIB positron emission tomography imaging, clinical examination, and cognitive testing. The binding potential (BP) of PIB for predefined regions and the mean cortical BP (MCBP) were calculated for each participant. Annual longitudinal follow‐up and postmortem examinations were performed on a subset of participants. Regional PIB BPs and the proportion of individuals with abnormally elevated MCBP were not significantly different across participant groups. Elevated PIB binding was associated with worse global cognitive impairment in participants with Lewy body disorders but was not associated with any other clinical or neuropsychological features, including earlier onset or faster rate of progression of cognitive impairment. These results suggest that the presence of fibrillar amyloid‐β does not distinguish between clinical subtypes of Lewy body‐associated disorders, although larger numbers are needed to more definitively rule out this association. Amyloid‐β may modify the severity of global cognitive impairment in individuals with Lewy body‐associated dementia. © 2010 Movement Disorder Society
Url:
DOI: 10.1002/mds.23393
Affiliations:
- États-Unis
- Missouri (État)
- Saint-Louis (Missouri)
- École de médecine (Université Washington de Saint-Louis)
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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="2010-11-15">2010-11-15</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">15</biblScope><biblScope unit="page" from="2516">2516</biblScope><biblScope unit="page" to="2523">2523</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">9C2EDC9AEAFC1C67DF8758BD60671C96B5845640</idno><idno type="DOI">10.1002/mds.23393</idno><idno type="ArticleID">MDS23393</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>PET</term><term>Parkinson's disease</term><term>Parkinson's disease with dementia</term><term>dementia with Lewy bodies</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Clinicopathologic studies of Parkinson disease dementia (PDD) and dementia with Lewy bodies (DLB) commonly reveal abnormal β‐amyloid deposition in addition to diffuse Lewy bodies (α‐synuclein aggregates), but the relationship among these neuropathologic features and the development of dementia in these disorders remains uncertain. The purpose of this study was to determine whether amyloid‐β deposition detected by PET imaging with Pittsburgh Compound B (PIB) distinguishes clinical subtypes of Lewy body‐associated disorders. Nine healthy controls, 8 PD with no cognitive impairment, 9 PD with mild cognitive impairment, 6 DLB, and 15 PDD patients underwent [11C]‐PIB positron emission tomography imaging, clinical examination, and cognitive testing. The binding potential (BP) of PIB for predefined regions and the mean cortical BP (MCBP) were calculated for each participant. Annual longitudinal follow‐up and postmortem examinations were performed on a subset of participants. Regional PIB BPs and the proportion of individuals with abnormally elevated MCBP were not significantly different across participant groups. Elevated PIB binding was associated with worse global cognitive impairment in participants with Lewy body disorders but was not associated with any other clinical or neuropsychological features, including earlier onset or faster rate of progression of cognitive impairment. These results suggest that the presence of fibrillar amyloid‐β does not distinguish between clinical subtypes of Lewy body‐associated disorders, although larger numbers are needed to more definitively rule out this association. Amyloid‐β may modify the severity of global cognitive impairment in individuals with Lewy body‐associated dementia. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Missouri (État)</li></region><settlement><li>Saint-Louis (Missouri)</li></settlement><orgName><li>École de médecine (Université Washington de Saint-Louis)</li></orgName></list><tree><country name="États-Unis"><region name="Missouri (État)"><name sortKey="Foster, Erin R" sort="Foster, Erin R" uniqKey="Foster E" first="Erin R." last="Foster">Erin R. Foster</name></region><name sortKey="Burack, Michelle A" sort="Burack, Michelle A" uniqKey="Burack M" first="Michelle A." last="Burack">Michelle A. Burack</name><name sortKey="Burack, Michelle A" sort="Burack, Michelle A" uniqKey="Burack M" first="Michelle A." last="Burack">Michelle A. Burack</name><name sortKey="Cairns, Nigel J" sort="Cairns, Nigel J" uniqKey="Cairns N" first="Nigel J." last="Cairns">Nigel J. Cairns</name><name sortKey="Cairns, Nigel J" sort="Cairns, Nigel J" uniqKey="Cairns N" first="Nigel J." last="Cairns">Nigel J. Cairns</name><name sortKey="Campbell, Meghan C" sort="Campbell, Meghan C" uniqKey="Campbell M" first="Meghan C." last="Campbell">Meghan C. Campbell</name><name sortKey="Flores, Hubert P" sort="Flores, Hubert P" uniqKey="Flores H" first="Hubert P." last="Flores">Hubert P. Flores</name><name sortKey="Foster, Erin R" sort="Foster, Erin R" uniqKey="Foster E" first="Erin R." last="Foster">Erin R. Foster</name><name sortKey="Foster, Erin R" sort="Foster, Erin R" uniqKey="Foster E" first="Erin R." last="Foster">Erin R. Foster</name><name sortKey="Hartlein, Johanna" sort="Hartlein, Johanna" uniqKey="Hartlein J" first="Johanna" last="Hartlein">Johanna Hartlein</name><name sortKey="Hershey, Tamara" sort="Hershey, Tamara" uniqKey="Hershey T" first="Tamara" last="Hershey">Tamara Hershey</name><name sortKey="Hershey, Tamara" sort="Hershey, Tamara" uniqKey="Hershey T" first="Tamara" last="Hershey">Tamara Hershey</name><name sortKey="Hershey, Tamara" sort="Hershey, Tamara" uniqKey="Hershey T" first="Tamara" last="Hershey">Tamara Hershey</name><name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name><name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name><name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name><name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name><name sortKey="Perlmutter, Joel S" sort="Perlmutter, Joel S" uniqKey="Perlmutter J" first="Joel S." last="Perlmutter">Joel S. Perlmutter</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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