001     835091
005     20210129230819.0
024 7 _ |a 10.1001/jamaneurol.2017.0892
|2 doi
024 7 _ |a 0003-9942
|2 ISSN
024 7 _ |a 0375-8540
|2 ISSN
024 7 _ |a 1538-3687
|2 ISSN
024 7 _ |a 2168-6149
|2 ISSN
024 7 _ |a 2168-6157
|2 ISSN
024 7 _ |a 2128/14936
|2 Handle
024 7 _ |a WOS:000405077100015
|2 WOS
024 7 _ |a altmetric:20705924
|2 altmetric
024 7 _ |a pmid:28558099
|2 pmid
037 _ _ |a FZJ-2017-04959
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Farrell, Michelle E.
|0 P:(DE-HGF)0
|b 0
245 _ _ |a Association of Longitudinal Cognitive Decline With Amyloid Burden in Middle-aged and Older Adults
260 _ _ |a Chicago, Ill.
|c 2017
|b American Medical Association
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1500536913_11986
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Importance Presently, the clinical standard for reporting the results of an amyloid positron emission tomography scan is to assign a dichotomous rating of positive or negative for the presence of amyloid. In a 4-year longitudinal study, we investigated whether using a continuous measure of the magnitude of baseline amyloid burden would provide valuable information about the rate of future cognitive decline over the subsequent 4 years compared with a dichotomous measure in middle-aged and older adults.Objective To examine whether a continuous, dose-response relationship between amyloid burden and cognitive decline was present among middle-aged and older adults.Design, Setting, and Participants This cohort study included 174 participants from the Dallas Lifespan Brain Study who were 40 to 89 years old at the beginning of the study, were cognitively normal at baseline (a Mini-Mental State Examination score of 26 or higher) with no history of neurological or psychiatric disorders, and had completed amyloid imaging ([18F]-florbetapir) at baseline and cognitive assessments at baseline and a 4-year follow-up. Continuous amyloid burden was measured as the mean cortical standardized uptake value ratio (SUVR) at baseline.Main Outcomes and Measures Linear mixed models assessed the effect of increasing baseline amyloid over time (SUVR × time interaction) on episodic memory, reasoning, processing speed, vocabulary, and Mini-Mental State Examination performance. Age, sex, education, apolipoprotein ε4, and the random effect of intercepts were included as covariates.Results The mean (SD) age for all participants (n = 174) was 66.44 (11.74) years, and 65 participants (37%) were men. The primary analyses yielded significant SUVR × time interactions in episodic memory, processing speed, vocabulary, and Mini-Mental State Examination performance, but not in reasoning performance. Higher baseline SUVR projected greater cognitive decline over 4 years. When controlling for variance related to a dichotomized positive/negative classification, most effects on cognition remained. Dichotomized amyloid status alone yielded fewer significant effects of amyloid on cognitive decline than continuous SUVR. Among amyloid-positive participants, increasing baseline SUVR predicted an increasing decline in episodic memory, but other effects on cognition were more limited. Finally, higher baseline amyloid burden among middle-aged adults was related to changes in vocabulary, with the effect driven by 3 apolipoprotein ε4 homozygotes.Conclusions and Relevance These results suggest that the magnitude of amyloid burden at baseline is associated with the rate of cognitive decline over 4 years and potentially provides important information about the rate of future cognitive decline that is not available from a dichotomous positive/negative categorization.
536 _ _ |a 572 - (Dys-)function and Plasticity (POF3-572)
|0 G:(DE-HGF)POF3-572
|c POF3-572
|f POF III
|x 0
588 _ _ |a Dataset connected to CrossRef
700 1 _ |a Kennedy, Kristen M.
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Rodrigue, Karen M.
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Wig, Gagan
|0 P:(DE-HGF)0
|b 3
700 1 _ |a Bischof, Gérard N.
|0 P:(DE-Juel1)166265
|b 4
700 1 _ |a Rieck, Jennifer R.
|0 P:(DE-HGF)0
|b 5
700 1 _ |a Chen, Xi
|0 P:(DE-HGF)0
|b 6
700 1 _ |a Festini, Sara B.
|0 P:(DE-HGF)0
|b 7
700 1 _ |a Devous, Michael D.
|0 P:(DE-HGF)0
|b 8
700 1 _ |a Park, Denise C.
|0 P:(DE-HGF)0
|b 9
|e Corresponding author
773 _ _ |a 10.1001/jamaneurol.2017.0892
|g Vol. 74, no. 7, p. 830 -
|0 PERI:(DE-600)2701924-X
|n 7
|p 830 - 838
|t JAMA neurology
|v 74
|y 2017
|x 2168-6149
856 4 _ |u https://juser.fz-juelich.de/record/835091/files/jamaneurology_Farrell_2017_oi_170026.pdf
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/835091/files/jamaneurology_Farrell_2017_oi_170026.gif?subformat=icon
|x icon
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/835091/files/jamaneurology_Farrell_2017_oi_170026.jpg?subformat=icon-1440
|x icon-1440
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/835091/files/jamaneurology_Farrell_2017_oi_170026.jpg?subformat=icon-180
|x icon-180
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/835091/files/jamaneurology_Farrell_2017_oi_170026.jpg?subformat=icon-640
|x icon-640
|y OpenAccess
856 4 _ |u https://juser.fz-juelich.de/record/835091/files/jamaneurology_Farrell_2017_oi_170026.pdf?subformat=pdfa
|x pdfa
|y OpenAccess
909 C O |o oai:juser.fz-juelich.de:835091
|p openaire
|p open_access
|p driver
|p VDB
|p dnbdelivery
910 1 _ |a Forschungszentrum Jülich
|0 I:(DE-588b)5008462-8
|k FZJ
|b 4
|6 P:(DE-Juel1)166265
913 1 _ |a DE-HGF
|b Key Technologies
|l Decoding the Human Brain
|1 G:(DE-HGF)POF3-570
|0 G:(DE-HGF)POF3-572
|2 G:(DE-HGF)POF3-500
|v (Dys-)function and Plasticity
|x 0
|4 G:(DE-HGF)POF
|3 G:(DE-HGF)POF3
914 1 _ |y 2017
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1030
|2 StatID
|b Current Contents - Life Sciences
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b JAMA NEUROL : 2015
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
915 _ _ |a WoS
|0 StatID:(DE-HGF)0110
|2 StatID
|b Science Citation Index
915 _ _ |a WoS
|0 StatID:(DE-HGF)0111
|2 StatID
|b Science Citation Index Expanded
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b JAMA NEUROL : 2015
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0310
|2 StatID
|b NCBI Molecular Biology Database
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1110
|2 StatID
|b Current Contents - Clinical Medicine
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Thomson Reuters Master Journal List
920 _ _ |l yes
920 1 _ |0 I:(DE-Juel1)INM-3-20090406
|k INM-3
|l Kognitive Neurowissenschaften
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-Juel1)INM-3-20090406
980 1 _ |a FullTexts


LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21