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000165167 037__ $$aDZNE-2022-01469
000165167 041__ $$aEnglish
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000165167 1001_ $$aStrain, Jeremy F$$b0
000165167 245__ $$aCovariance-based vs. correlation-based functional connectivity dissociates healthy aging from Alzheimer disease.
000165167 260__ $$aOrlando, Fla.$$bAcademic Press$$c2022
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000165167 520__ $$aPrior studies of aging and Alzheimer disease have evaluated resting state functional connectivity (FC) using either seed-based correlation (SBC) or independent component analysis (ICA), with a focus on particular functional systems. SBC and ICA both are insensitive to differences in signal amplitude. At the same time, accumulating evidence indicates that the amplitude of spontaneous BOLD signal fluctuations is physiologically meaningful. We systematically compared covariance-based FC, which is sensitive to amplitude, vs. correlation-based FC, which is not, in affected individuals and controls drawn from two cohorts of participants including autosomal dominant Alzheimer disease (ADAD), late onset Alzheimer disease (LOAD), and age-matched controls. Functional connectivity was computed over 222 regions of interest and group differences were evaluated in terms of components projected onto a space of lower dimension. Our principal observations are: (1) Aging is associated with global loss of resting state fMRI signal amplitude that is approximately uniform across resting state networks. (2) Thus, covariance FC measures decrease with age whereas correlation FC is relatively preserved in healthy aging. (3) In contrast, symptomatic ADAD and LOAD both lead to loss of spontaneous activity amplitude as well as severely degraded correlation structure. These results demonstrate a double dissociation between age vs. Alzheimer disease and the amplitude vs. correlation structure of resting state BOLD signals. Modeling results suggest that the AD-associated loss of correlation structure is attributable to a relative increase in the fraction of locally restricted as opposed to widely shared variance.
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000165167 650_7 $$2Other$$aAging
000165167 650_7 $$2Other$$aAutosomal dominant Alzheimer disease
000165167 650_7 $$2Other$$aCovariance
000165167 650_7 $$2Other$$aLate onset Alzheimer disease
000165167 650_7 $$2Other$$aResting-state functional connectivity
000165167 650_2 $$2MeSH$$aAging
000165167 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000165167 650_2 $$2MeSH$$aBrain: physiology
000165167 650_2 $$2MeSH$$aHealthy Aging
000165167 650_2 $$2MeSH$$aHumans
000165167 650_2 $$2MeSH$$aMagnetic Resonance Imaging: methods
000165167 7001_ $$aBrier, Matthew R$$b1
000165167 7001_ $$aTanenbaum, Aaron$$b2
000165167 7001_ $$aGordon, Brian A$$b3
000165167 7001_ $$aMcCarthy, John E$$b4
000165167 7001_ $$aDincer, Aylin$$b5
000165167 7001_ $$aMarcus, Daniel S$$b6
000165167 7001_ $$aChhatwal, Jasmeer P$$b7
000165167 7001_ $$aGraff-Radford, Neill R$$b8
000165167 7001_ $$aDay, Gregory S$$b9
000165167 7001_ $$0P:(DE-2719)9000177$$ala Fougère, Christian$$b10$$udzne
000165167 7001_ $$aPerrin, Richard J$$b11
000165167 7001_ $$aSalloway, Stephen$$b12
000165167 7001_ $$aSchofield, Peter R$$b13
000165167 7001_ $$0P:(DE-2719)9000355$$aYakushev, Igor$$b14$$udzne
000165167 7001_ $$aIkeuchi, Takeshi$$b15
000165167 7001_ $$0P:(DE-2719)2811820$$aVöglein, Jonathan$$b16$$udzne
000165167 7001_ $$aMorris, John C$$b17
000165167 7001_ $$aBenzinger, Tammie L S$$b18
000165167 7001_ $$aBateman, Randall J$$b19
000165167 7001_ $$aAnces, Beau M$$b20
000165167 7001_ $$aSnyder, Abraham Z$$b21
000165167 7001_ $$aNetwork, Dominantly Inherited Alzheimer$$b22$$eCollaboration Author
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