Home > Publications Database > Left frontal cortex connectivity underlies cognitive reserve in prodromal Alzheimer disease. > print

001     139148
005     20240321220550.0
024 7 _ |a 10.1212/WNL.0000000000003711
|2 doi
024 7 _ |a pmid:28188306
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024 7 _ |a pmc:PMC5384837
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024 7 _ |a 0028-3878
|2 ISSN
024 7 _ |a 1526-632X
|2 ISSN
024 7 _ |a altmetric:16318423
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037 _ _ |a DZNE-2020-05470
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Franzmeier, Nicolai
|0 P:(DE-HGF)0
|b 0
245 _ _ |a Left frontal cortex connectivity underlies cognitive reserve in prodromal Alzheimer disease.
260 _ _ |a [S.l.]
|c 2017
|b Ovid
264 _ 1 |3 online
|2 Crossref
|b Ovid Technologies (Wolters Kluwer Health)
|c 2017-02-10
264 _ 1 |3 print
|2 Crossref
|b Ovid Technologies (Wolters Kluwer Health)
|c 2017-03-14
336 7 _ |a article
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336 7 _ |a Output Types/Journal article
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336 7 _ |a Journal Article
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|s 1587036213_2267
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336 7 _ |a ARTICLE
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336 7 _ |a JOURNAL_ARTICLE
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336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a To 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.
536 _ _ |a 344 - Clinical and Health Care Research (POF3-344)
|0 G:(DE-HGF)POF3-344
|c POF3-344
|f POF III
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588 _ _ |a Dataset connected to CrossRef, PubMed,
650 _ 7 |a Fluorodeoxyglucose F18
|0 0Z5B2CJX4D
|2 NLM Chemicals
650 _ 7 |a Oxygen
|0 S88TT14065
|2 NLM Chemicals
650 _ 2 |a Alzheimer Disease: complications
|2 MeSH
650 _ 2 |a Alzheimer Disease: diagnostic imaging
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Chi-Square Distribution
|2 MeSH
650 _ 2 |a Cognition Disorders: etiology
|2 MeSH
650 _ 2 |a Cognitive Reserve: physiology
|2 MeSH
650 _ 2 |a Epilepsy: diagnostic imaging
|2 MeSH
650 _ 2 |a Epilepsy: etiology
|2 MeSH
650 _ 2 |a Female
|2 MeSH
650 _ 2 |a Fluorodeoxyglucose F18: metabolism
|2 MeSH
650 _ 2 |a Frontal Lobe: diagnostic imaging
|2 MeSH
650 _ 2 |a Frontal Lobe: pathology
|2 MeSH
650 _ 2 |a Functional Laterality: physiology
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Magnetic Resonance Imaging
|2 MeSH
650 _ 2 |a Male
|2 MeSH
650 _ 2 |a Nerve Net: pathology
|2 MeSH
650 _ 2 |a Neuropsychological Tests
|2 MeSH
650 _ 2 |a Oxygen: blood
|2 MeSH
650 _ 2 |a Positron-Emission Tomography
|2 MeSH
650 _ 2 |a Prodromal Symptoms
|2 MeSH
700 1 _ |a Duering, Marco
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Weiner, Michael
|0 P:(DE-HGF)0
|b 2
700 1 _ |a Dichgans, Martin
|0 P:(DE-2719)2000030
|b 3
|u dzne
700 1 _ |a Ewers, Michael
|0 P:(DE-HGF)0
|b 4
|e Corresponding author
700 1 _ |a Initiative, Alzheimer's Disease Neuroimaging
|0 P:(DE-HGF)0
|b 5
773 1 8 |a 10.1212/wnl.0000000000003711
|b : Ovid Technologies (Wolters Kluwer Health), 2017-02-10
|n 11
|p 1054-1061
|3 journal-article
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|t Neurology
|v 88
|y 2017
|x 0028-3878
773 _ _ |a 10.1212/WNL.0000000000003711
|g Vol. 88, no. 11, p. 1054 - 1061
|0 PERI:(DE-600)1491874-2
|n 11
|q 88:11<1054 - 1061
|p 1054-1061
|t Neurology
|v 88
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|x 0028-3878
856 7 _ |2 Pubmed Central
|u http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384837
909 C O |o oai:pub.dzne.de:139148
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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914 1 _ |y 2017
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