Increased posterior default mode network activity and structural connectivity in young adult APOE -ε4 carriers: a multi-modal imaging investigation
Carl J. Hodgetts, Jonathan P. Shine, Huw Williams, Mark Postans, Rebecca Sims, Julie Williams, Andrew Lawrence, Kim S. Graham
bioRxiv March 22, 2018 preprint DOI: 10.1101/285536 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Cross-sectional observational study |
|---|---|
| Sample size | 30 |
| Population | Young adults, mean age 20 years; half APOE-ε4 carriers, half APOE-ε3ε3/ε2ε3 non-carriers |
| Topics | Default mode network |
| Key findings | APOE-ε4 carriers had lower mean diffusivity and higher fractional anisotropy in the parahippocampal cingulum bundle than non-carriers, and this microstructure was selectively associated with posterior default mode network activity during a scene discrimination task. The authors argue these findings support a lifespan view in which early-life brain changes in vulnerable networks may increase neural activity and ultimately trigger amyloid-β deposition. |
Abstract
Young adult APOE -ε4 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 (half APOE -ε4 carriers, the other half APOE -ε3ε3/ε2ε3; mean age 20 years) were scanned using both diffusion and functional magnetic resonance imaging. Diffusion tractography was used to quantify the microstructure (mean diffusivity, MD; fractional anisotropy, FA) of the parahippocampal cingulum bundle (PHCB), which links pDMN and the medial temporal lobe. APOE -ε4 carriers had lower MD and higher FA relative to non-carriers in PHCB. Further, PHCB microstructure was selectively associated with pDMN activity during a scene discrimination task known to be sensitive to Alzheimer’s disease (AD). These findings are consistent with a lifespan view of AD risk, where early-life structural and functional brain changes in specific, vulnerable networks leads to increased neural activity that may ultimately trigger amyloid-ß deposition.
Comparable studies
Other cross-sectional and survey studies on default mode network, most cited first.