Regional brain amyloid-[beta] accumulation associates with domain-specific cognitive performance in Parkinson disease without dementia
Parkinson disease patients develop clinically significant cognitive impairment at variable times over their disease course, which is often preceded by milder deficits in memory, visuo-spatial, and executive domains. The significance of amyloid-[beta] accumulation to these problems is unclear. We hyp...
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Veröffentlicht in: | PloS one 2017-05, Vol.12 (5), p.e0177924 |
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creator | Chen-Plotkin, Alice S Nasrallah, Ilya M Weintraub, Daniel Chen, Yin J Akhtar, Rizwan S Van Deerlin, Vivianna M Gross, Rachel G Trojanowski, John Q Dubroff, Jacob G Xie, Sharon X Siderowf, Andrew D Hurtig, Howard I Rick, Jacqueline |
description | Parkinson disease patients develop clinically significant cognitive impairment at variable times over their disease course, which is often preceded by milder deficits in memory, visuo-spatial, and executive domains. The significance of amyloid-[beta] accumulation to these problems is unclear. We hypothesized that amyloid-[beta] PET imaging by .sup.18 F-florbetapir, a radiotracer that detects fibrillar amyloid-[beta] plaque deposits, would identify subjects with global cognitive impairment or poor performance in individual cognitive domains in non-demented Parkinson disease patients. We assessed 61 non-demented Parkinson disease patients with detailed cognitive assessments and .sup.18 F-florbetapir PET brain imaging. Scans were interpreted qualitatively (positive or negative) by two independent nuclear medicine physicians blinded to clinical data, and quantitatively by a novel volume-weighted method. The presence of mild cognitive impairment was determined through an expert consensus process using Level 1 criteria from the Movement Disorder Society. Nineteen participants (31.2%) were diagnosed with mild cognitive impairment and the remainder had normal cognition. Qualitative .sup.18 F-florbetapir PET imaging was positive in 15 participants (24.6%). Increasing age and presence of an APOE [epsilon]4 allele were associated with higher composite .sup.18 F-florbetapir binding. In multivariable models, an abnormal .sup.18 F-florbetapir scan by expert rating was not associated with a diagnosis of mild cognitive impairment. However, .sup.18 F-florbetapir retention values in the posterior cingulate gyrus inversely correlated with verbal memory performance. Retention values in the frontal cortex, precuneus, and anterior cingulate gyrus retention values inversely correlated with naming performance. Regional cortical amyloid-[beta] amyloid, as measured by .sup.18 F-florbetapir PET, may be a biomarker of specific cognitive deficits in non-demented Parkinson disease patients. |
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The significance of amyloid-[beta] accumulation to these problems is unclear. We hypothesized that amyloid-[beta] PET imaging by .sup.18 F-florbetapir, a radiotracer that detects fibrillar amyloid-[beta] plaque deposits, would identify subjects with global cognitive impairment or poor performance in individual cognitive domains in non-demented Parkinson disease patients. We assessed 61 non-demented Parkinson disease patients with detailed cognitive assessments and .sup.18 F-florbetapir PET brain imaging. Scans were interpreted qualitatively (positive or negative) by two independent nuclear medicine physicians blinded to clinical data, and quantitatively by a novel volume-weighted method. The presence of mild cognitive impairment was determined through an expert consensus process using Level 1 criteria from the Movement Disorder Society. Nineteen participants (31.2%) were diagnosed with mild cognitive impairment and the remainder had normal cognition. Qualitative .sup.18 F-florbetapir PET imaging was positive in 15 participants (24.6%). Increasing age and presence of an APOE [epsilon]4 allele were associated with higher composite .sup.18 F-florbetapir binding. In multivariable models, an abnormal .sup.18 F-florbetapir scan by expert rating was not associated with a diagnosis of mild cognitive impairment. However, .sup.18 F-florbetapir retention values in the posterior cingulate gyrus inversely correlated with verbal memory performance. Retention values in the frontal cortex, precuneus, and anterior cingulate gyrus retention values inversely correlated with naming performance. Regional cortical amyloid-[beta] amyloid, as measured by .sup.18 F-florbetapir PET, may be a biomarker of specific cognitive deficits in non-demented Parkinson disease patients.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0177924</identifier><language>eng</language><publisher>Public Library of Science</publisher><subject>Amyloid beta-protein ; Analysis ; Cognition ; Parkinson disease ; Positron emission tomography</subject><ispartof>PloS one, 2017-05, Vol.12 (5), p.e0177924</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,27901,27902</link.rule.ids></links><search><creatorcontrib>Chen-Plotkin, Alice S</creatorcontrib><creatorcontrib>Nasrallah, Ilya M</creatorcontrib><creatorcontrib>Weintraub, Daniel</creatorcontrib><creatorcontrib>Chen, Yin J</creatorcontrib><creatorcontrib>Akhtar, Rizwan S</creatorcontrib><creatorcontrib>Van Deerlin, Vivianna M</creatorcontrib><creatorcontrib>Gross, Rachel G</creatorcontrib><creatorcontrib>Trojanowski, John Q</creatorcontrib><creatorcontrib>Dubroff, Jacob G</creatorcontrib><creatorcontrib>Xie, Sharon X</creatorcontrib><creatorcontrib>Siderowf, Andrew D</creatorcontrib><creatorcontrib>Hurtig, Howard I</creatorcontrib><creatorcontrib>Rick, Jacqueline</creatorcontrib><title>Regional brain amyloid-[beta] accumulation associates with domain-specific cognitive performance in Parkinson disease without dementia</title><title>PloS one</title><description>Parkinson disease patients develop clinically significant cognitive impairment at variable times over their disease course, which is often preceded by milder deficits in memory, visuo-spatial, and executive domains. The significance of amyloid-[beta] accumulation to these problems is unclear. We hypothesized that amyloid-[beta] PET imaging by .sup.18 F-florbetapir, a radiotracer that detects fibrillar amyloid-[beta] plaque deposits, would identify subjects with global cognitive impairment or poor performance in individual cognitive domains in non-demented Parkinson disease patients. We assessed 61 non-demented Parkinson disease patients with detailed cognitive assessments and .sup.18 F-florbetapir PET brain imaging. Scans were interpreted qualitatively (positive or negative) by two independent nuclear medicine physicians blinded to clinical data, and quantitatively by a novel volume-weighted method. The presence of mild cognitive impairment was determined through an expert consensus process using Level 1 criteria from the Movement Disorder Society. Nineteen participants (31.2%) were diagnosed with mild cognitive impairment and the remainder had normal cognition. Qualitative .sup.18 F-florbetapir PET imaging was positive in 15 participants (24.6%). Increasing age and presence of an APOE [epsilon]4 allele were associated with higher composite .sup.18 F-florbetapir binding. In multivariable models, an abnormal .sup.18 F-florbetapir scan by expert rating was not associated with a diagnosis of mild cognitive impairment. However, .sup.18 F-florbetapir retention values in the posterior cingulate gyrus inversely correlated with verbal memory performance. Retention values in the frontal cortex, precuneus, and anterior cingulate gyrus retention values inversely correlated with naming performance. Regional cortical amyloid-[beta] amyloid, as measured by .sup.18 F-florbetapir PET, may be a biomarker of specific cognitive deficits in non-demented Parkinson disease patients.</description><subject>Amyloid beta-protein</subject><subject>Analysis</subject><subject>Cognition</subject><subject>Parkinson disease</subject><subject>Positron emission tomography</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid/><recordid>eNpNkE9LwzAYh4MoOKffwENA8NaZpEnbHMfQKQwU2U1kvE3fdpltMppU8Qv4ua1_Dju9v8PzPIeXkEvOZjzN-c3OD72Ddrb3DmeM57kW8ohMuE5FkgmWHh_sU3IWwo4xlRZZNiFfz9hYP8q07ME6Ct1n622VvJQY4ZWCMUM3tBBHhkII3liIGOiHjVta-W5UkrBHY2trqPGNs9G-I91jX_u-A2eQjtEn6N-sC2OisgEh4K_vh0gr7NBFC-fkpIY24MX_nZL13e16cZ-sHpcPi_kqaZTmiYRMM13zmglUWhlU0qRKKmO0UTrLIdeqrrASUBaZrGShOSt4ybgUQmEm0ym5-ss20OLGutrHHkxng9nMpRaF4LrgI3V9QG0R2rgNvh1-nhAOwW8rUHVA</recordid><startdate>20170525</startdate><enddate>20170525</enddate><creator>Chen-Plotkin, Alice S</creator><creator>Nasrallah, Ilya M</creator><creator>Weintraub, Daniel</creator><creator>Chen, Yin J</creator><creator>Akhtar, Rizwan S</creator><creator>Van Deerlin, Vivianna M</creator><creator>Gross, Rachel G</creator><creator>Trojanowski, John Q</creator><creator>Dubroff, Jacob G</creator><creator>Xie, Sharon X</creator><creator>Siderowf, Andrew D</creator><creator>Hurtig, Howard I</creator><creator>Rick, Jacqueline</creator><general>Public Library of Science</general><scope/></search><sort><creationdate>20170525</creationdate><title>Regional brain amyloid-[beta] accumulation associates with domain-specific cognitive performance in Parkinson disease without dementia</title><author>Chen-Plotkin, Alice S ; Nasrallah, Ilya M ; Weintraub, Daniel ; Chen, Yin J ; Akhtar, Rizwan S ; Van Deerlin, Vivianna M ; Gross, Rachel G ; Trojanowski, John Q ; Dubroff, Jacob G ; Xie, Sharon X ; Siderowf, Andrew D ; Hurtig, Howard I ; Rick, Jacqueline</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-g591-4a6909f1f02e595ce54c3545cc9c5967a795fded2ab864d4891081b014225e643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Amyloid beta-protein</topic><topic>Analysis</topic><topic>Cognition</topic><topic>Parkinson disease</topic><topic>Positron emission tomography</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chen-Plotkin, Alice S</creatorcontrib><creatorcontrib>Nasrallah, Ilya M</creatorcontrib><creatorcontrib>Weintraub, Daniel</creatorcontrib><creatorcontrib>Chen, Yin J</creatorcontrib><creatorcontrib>Akhtar, Rizwan S</creatorcontrib><creatorcontrib>Van Deerlin, Vivianna M</creatorcontrib><creatorcontrib>Gross, Rachel G</creatorcontrib><creatorcontrib>Trojanowski, John Q</creatorcontrib><creatorcontrib>Dubroff, Jacob G</creatorcontrib><creatorcontrib>Xie, Sharon X</creatorcontrib><creatorcontrib>Siderowf, Andrew D</creatorcontrib><creatorcontrib>Hurtig, Howard I</creatorcontrib><creatorcontrib>Rick, Jacqueline</creatorcontrib><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen-Plotkin, Alice S</au><au>Nasrallah, Ilya M</au><au>Weintraub, Daniel</au><au>Chen, Yin J</au><au>Akhtar, Rizwan S</au><au>Van Deerlin, Vivianna M</au><au>Gross, Rachel G</au><au>Trojanowski, John Q</au><au>Dubroff, Jacob G</au><au>Xie, Sharon X</au><au>Siderowf, Andrew D</au><au>Hurtig, Howard I</au><au>Rick, Jacqueline</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regional brain amyloid-[beta] accumulation associates with domain-specific cognitive performance in Parkinson disease without dementia</atitle><jtitle>PloS one</jtitle><date>2017-05-25</date><risdate>2017</risdate><volume>12</volume><issue>5</issue><spage>e0177924</spage><pages>e0177924-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Parkinson disease patients develop clinically significant cognitive impairment at variable times over their disease course, which is often preceded by milder deficits in memory, visuo-spatial, and executive domains. The significance of amyloid-[beta] accumulation to these problems is unclear. We hypothesized that amyloid-[beta] PET imaging by .sup.18 F-florbetapir, a radiotracer that detects fibrillar amyloid-[beta] plaque deposits, would identify subjects with global cognitive impairment or poor performance in individual cognitive domains in non-demented Parkinson disease patients. We assessed 61 non-demented Parkinson disease patients with detailed cognitive assessments and .sup.18 F-florbetapir PET brain imaging. Scans were interpreted qualitatively (positive or negative) by two independent nuclear medicine physicians blinded to clinical data, and quantitatively by a novel volume-weighted method. The presence of mild cognitive impairment was determined through an expert consensus process using Level 1 criteria from the Movement Disorder Society. Nineteen participants (31.2%) were diagnosed with mild cognitive impairment and the remainder had normal cognition. Qualitative .sup.18 F-florbetapir PET imaging was positive in 15 participants (24.6%). Increasing age and presence of an APOE [epsilon]4 allele were associated with higher composite .sup.18 F-florbetapir binding. In multivariable models, an abnormal .sup.18 F-florbetapir scan by expert rating was not associated with a diagnosis of mild cognitive impairment. However, .sup.18 F-florbetapir retention values in the posterior cingulate gyrus inversely correlated with verbal memory performance. Retention values in the frontal cortex, precuneus, and anterior cingulate gyrus retention values inversely correlated with naming performance. Regional cortical amyloid-[beta] amyloid, as measured by .sup.18 F-florbetapir PET, may be a biomarker of specific cognitive deficits in non-demented Parkinson disease patients.</abstract><pub>Public Library of Science</pub><doi>10.1371/journal.pone.0177924</doi></addata></record> |
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subjects | Amyloid beta-protein Analysis Cognition Parkinson disease Positron emission tomography |
title | Regional brain amyloid-[beta] accumulation associates with domain-specific cognitive performance in Parkinson disease without dementia |
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