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000139148 0247_ $$2pmc$$apmc:PMC5384837
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000139148 0247_ $$2ISSN$$a1526-632X
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000139148 041__ $$aEnglish
000139148 082__ $$a610
000139148 1001_ $$0P:(DE-HGF)0$$aFranzmeier, Nicolai$$b0
000139148 245__ $$aLeft frontal cortex connectivity underlies cognitive reserve in prodromal Alzheimer disease.
000139148 260__ $$a[S.l.]$$bOvid$$c2017
000139148 264_1 $$2Crossref$$3online$$bOvid Technologies (Wolters Kluwer Health)$$c2017-02-10
000139148 264_1 $$2Crossref$$3print$$bOvid Technologies (Wolters Kluwer Health)$$c2017-03-14
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000139148 520__ $$aTo test whether higher global functional connectivity of the left frontal cortex (LFC) in Alzheimer disease (AD) is associated with more years of education (a proxy of cognitive reserve [CR]) and mitigates the association between AD-related fluorodeoxyglucose (FDG)-PET hypometabolism and episodic memory.Forty-four amyloid-PET-positive patients with amnestic mild cognitive impairment (MCI-Aβ+) and 24 amyloid-PET-negative healthy controls (HC) were included. Voxel-based linear regression analyses were used to test the association between years of education and FDG-PET in MCI-Aβ+, controlled for episodic memory performance. Global LFC (gLFC) connectivity was computed through seed-based resting-state fMRI correlations between the LFC (seed) and each voxel in the gray matter. In linear regression analyses, education as a predictor of gLFC connectivity and the interaction of gLFC connectivity × FDG-PET hypometabolism on episodic memory were tested.FDG-PET metabolism in the precuneus was reduced in MCI-Aβ+ compared to HC (p = 0.028), with stronger reductions observed in MCI-Aβ+ with more years of education (p = 0.006). In MCI-Aβ+, higher gLFC connectivity was associated with more years of education (p = 0.021). At higher levels of gLFC connectivity, the association between precuneus FDG-PET hypometabolism and lower memory performance was attenuated (p = 0.027).Higher gLFC connectivity is a functional substrate of CR that helps to maintain episodic memory relatively well in the face of emerging FDG-PET hypometabolism in early-stage AD.
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000139148 650_7 $$00Z5B2CJX4D$$2NLM Chemicals$$aFluorodeoxyglucose F18
000139148 650_7 $$0S88TT14065$$2NLM Chemicals$$aOxygen
000139148 650_2 $$2MeSH$$aAlzheimer Disease: complications
000139148 650_2 $$2MeSH$$aAlzheimer Disease: diagnostic imaging
000139148 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000139148 650_2 $$2MeSH$$aChi-Square Distribution
000139148 650_2 $$2MeSH$$aCognition Disorders: etiology
000139148 650_2 $$2MeSH$$aCognitive Reserve: physiology
000139148 650_2 $$2MeSH$$aEpilepsy: diagnostic imaging
000139148 650_2 $$2MeSH$$aEpilepsy: etiology
000139148 650_2 $$2MeSH$$aFemale
000139148 650_2 $$2MeSH$$aFluorodeoxyglucose F18: metabolism
000139148 650_2 $$2MeSH$$aFrontal Lobe: diagnostic imaging
000139148 650_2 $$2MeSH$$aFrontal Lobe: pathology
000139148 650_2 $$2MeSH$$aFunctional Laterality: physiology
000139148 650_2 $$2MeSH$$aHumans
000139148 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000139148 650_2 $$2MeSH$$aMale
000139148 650_2 $$2MeSH$$aNerve Net: pathology
000139148 650_2 $$2MeSH$$aNeuropsychological Tests
000139148 650_2 $$2MeSH$$aOxygen: blood
000139148 650_2 $$2MeSH$$aPositron-Emission Tomography
000139148 650_2 $$2MeSH$$aProdromal Symptoms
000139148 7001_ $$0P:(DE-HGF)0$$aDuering, Marco$$b1
000139148 7001_ $$0P:(DE-HGF)0$$aWeiner, Michael$$b2
000139148 7001_ $$0P:(DE-2719)2000030$$aDichgans, Martin$$b3$$udzne
000139148 7001_ $$0P:(DE-HGF)0$$aEwers, Michael$$b4$$eCorresponding author
000139148 7001_ $$0P:(DE-HGF)0$$aInitiative, Alzheimer's Disease Neuroimaging$$b5
000139148 77318 $$2Crossref$$3journal-article$$a10.1212/wnl.0000000000003711$$b : Ovid Technologies (Wolters Kluwer Health), 2017-02-10$$n11$$p1054-1061$$tNeurology$$v88$$x0028-3878$$y2017
000139148 773__ $$0PERI:(DE-600)1491874-2$$a10.1212/WNL.0000000000003711$$gVol. 88, no. 11, p. 1054 - 1061$$n11$$p1054-1061$$q88:11<1054 - 1061$$tNeurology$$v88$$x0028-3878$$y2017
000139148 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384837
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