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Updated: May 6, 2026

Network Analysis of the Default Mode Network Using Functional Connectivity MRI in Temporal Lobe Epilepsy
Published on: August 5, 2014
Amyloid-related default mode network hyperconnectivity and longitudinal decline in network distinctiveness in
Woo-Jin Cha1, Evgeny J Chumin2,3, Dahyun Yi4
1Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea.
Introduction:
We investigated stage-specific alterations in functional connectivity (FC) of the default mode network (DMN) across the Alzheimer's disease (AD) continuum and tested whether early amyloid beta (Aβ)-related changes in within-DMN FC (DMN-FCwithin) predicted longitudinal alterations in DMN between-network connectivity (DMN-FCbetween).
Methods:
Resting-state functional magnetic resonance imaging (fMRI) data were analyzed from 396 older adults: Aβ-negative cognitively normal (CN-, n = 213), Aβ-positive CN (CN+, n = 37), Aβ-positive mild cognitive impairment (MCI+, n = 72), and Aβ-positive dementia (dementia+, n = 74). Cross-sectional analyses compared DMN-FC across groups and examined associations with continuous Aβ burden at baseline. Longitudinal analyses in 171 CN participants with 2-year follow-up (CN-, n = 147; CN+, n = 24) tested whether baseline DMN-FCwithin predicted changes in DMN-FCbetween.
Results:
CN+ individuals showed elevated DMN-FCwithin and reduced DMN-FCbetween relative to other groups. In CN, Aβ burden was associated with FC, and baseline DMN-FCwithin predicted longitudinal increases in DMN-FCbetween only in CN+.
Discussion:
Aβ-related hyperconnectivity characterizes preclinical AD and may drive progressive network-level vulnerability.
Highlights:
Cognitively normal amyloid beta (Aβ)-positive (CN+) individuals showed stronger connectivity within the default mode network (DMN). CN+ individuals also showed weaker links between the DMN and other brain networks. Amyloid was not linked to connectivity changes in cognitively impaired adults. Higher DMN connectivity predicted broader network changes in CN+ individuals.
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