Journal
NEUROBIOLOGY OF AGING
Volume 73, Issue -, Pages 82-91Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.neurobiolaging.2018.08.026
Keywords
Alzheimer's disease; Default mode network; Diffusion MRI; Medial temporal lobe; Scene processing
Categories
Funding
- Alzheimer's Research UK
- Medical Research Council [MR/N01233X/1, G1002149]
- Wellcome Trust Strategic Award [104943/Z/14/Z]
- Waterloo Foundation
- Biotechnology and Biological Sciences Research Council [BB/I007091/1]
- Welsh Government via the Wales Institute of Cognitive Neuroscience
- BBSRC [BB/I007091/1] Funding Source: UKRI
- MRC [G0600237, MR/M009076/1, G0300429, MR/N01233X/1, MR/L023784/2, MR/L023784/1, G0902227, MR/P024696/1] Funding Source: UKRI
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Young adult APOE-epsilon 4 carriers show increased activity in posterior regions of the default mode network (pDMN), but how this is related to structural connectivity is unknown. Thirty young adults (one half of whom were APOE-epsilon 4 carriers; mean age 20 years) were scanned using both diffusion and functional magnetic resonance imaging. The parahippocampal cingulum bundle (PHCB)-which links the pDMN and the medial temporal lobe-was manually delineated in individual participants using deterministic tractography. Measures of tract microstructure (mean diffusivity and fractional anisotropy) were then extracted from these tract delineations.APOE-epsilon 4 carriers had lower mean diffusivity and higher fractional anisotropy relative to noncarriers in PHCB, but not in a control tract (the inferior longitudinal fasciculus). Furthermore, PHCB microstructure was selectively associated with pDMN (and medial temporal lobe) activity during a scene discrimination task known to be sensitive to Alzheimer's disease. These findings are consistent with a lifespan view of Alzheimer's disease risk, where early-life, connectivity-related changes in specific, vulnerable hubs (e.g., pDMN) lead to increased neural activity. Critically, such changes may reflect reduced network efficiency/flexibility in APOE-epsilon 4 carriers, which in itself may portend a faster decline in connectivity over the lifespan and ultimately trigger early amyloid-beta deposition in later life. (C) 2018 The Authors. Published by Elsevier Inc.
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