Journal
ALZHEIMERS & DEMENTIA
Volume 11, Issue 6, Pages 648-657Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jalz.2014.05.1755
Keywords
APOE gene; Alzheimer's disease; BOLD; Cerebrovascular reactivity; fMRI
Categories
Funding
- HDH Wills 1965 Charitable Trust [1117747]
- University of Oxford Clarendon Scholarship
- UK EPSRC [EP/G004277/1]
- Royal Society University Research Fellowship [UF080387]
- National Institute for Health Research (NIHR), UK as part of the Oxford Biomedical Research Centre (BRC)
- EPSRC [EP/G004277/1] Funding Source: UKRI
- MRC [G9409634, G1001354, G9409531, MR/M024903/1] Funding Source: UKRI
- Royal Society [UF080387] Funding Source: Royal Society
- Alzheimers Research UK [ARUK-PPG2012A-5] Funding Source: researchfish
- Engineering and Physical Sciences Research Council [EP/G004277/1] Funding Source: researchfish
- Medical Research Council [MR/M024903/1, G1001354, G9409531, G9409634] Funding Source: researchfish
- National Institute for Health Research [NF-SI-0514-10022] Funding Source: researchfish
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Background: Functional magnetic resonance imaging (MRI) studies have shown that APOE epsilon 2- and epsilon 4-carriers have similar patterns of blood-oxygenation-level-dependent (BOLD) activation suggesting that we need to look beyond the BOLD signal to link APOE's effect on the brain to Alzheimer's disease (AD)-risk. Methods: We evaluated APOE-related differences in BOLD activation in response to a memory task, cerebrovascular reactivity using a CO2-inhalation challenge (CO2-CVR), and the potential contribution of CO2-CVR to the BOLD signal. Results: APOE epsilon 4-carriers had the highest task-related hippocampal BOLD signal relative to non-carriers. The largest differences in CO2-CVR were between epsilon 2- and epsilon 4-carriers, with the latter having the lowest values. Genotype differences in CO2-CVR accounted for similar to 70% of hippocampal BOLD differences between groups. Conclusion: Because CO2-CVR gauges vascular health, the differential effect of APOE in young adults may reflect a vascular contribution to the vulnerability of epsilon 4-carriers to late-life pathology. Studies confirming our findings are warranted. (C) 2015 The Alzheimer's Association. Published by Elsevier Inc. All rights reserved.
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