Affiliations: [a]
Department of Psychology, University of Southern California, Los Angeles, CA, USA
| [b]
Institute for Memory Impairments and Neurological Disorders, University of California Irvine, Irvine, CA, USA
| [c]
Department of Psychological Science, University of California Irvine, Irvine, CA, USA
Correspondence:
[*]
Correspondence to: [*]Daniel A. Nation, PhD, Associate Professor, University of California Irvine, Department of Psychological Science, 4201 Social and Behavioral Sciences Gateway, Irvine, CA 92697-7085, USA. Tel.: +1 949 824 9339; E-mail: dnation@uci.edu.
Note: [1] 1Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (http://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at:http://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf.
Abstract: Background:Blood pressure variability (BPV) is associated with cognitive decline and Alzheimer’s disease (AD), but relationships with AD risk gene apolipoprotein (APOE) ɛ4 remain understudied. Objective:Examined the longitudinal relationship between BPV and cognitive change in APOE ɛ4 carriers and APOE ɛ3 homozygotes. Methods:1,194 Alzheimer’s Disease Neuroimaging Initiative participants (554 APOE ɛ4 carriers) underwent 3-4 blood pressure measurements between study baseline and 12-month follow-up. Visit-to-visit BPV was calculated as variability independent of mean over these 12 months. Participants subsequently underwent ≥1 neuropsychological exam at 12-month follow-up or later (up to 156 months later). Composite scores for the domains of memory, language, executive function, and visuospatial abilities were determined. Linear mixed models examined the 3-way interaction of BPV×APOE ɛ4 carrier status x time predicting change in composite scores. Results:Higher systolic BPV predicted greater decline in memory (+1 SD increase of BPV: β= –0.001, p < 0.001) and language (β= –0.002, p < 0.0001) among APOE ɛ4 carriers, but not APOE ɛ3 homozygotes (memory: +1 SD increase of BPV: β= 0.0001, p = 0.57; language: β= 0.0001, p = 0.72). Systolic BPV was not significantly associated with change in executive function or visuospatial abilities in APOE ɛ4 carriers (ps = 0.08–0.16) or APOE ɛ3 homozygotes (ps = 0.48–0.12). Conclusion:Cognitive decline associated with high BPV may be specifically accelerated among APOE ɛ4 carriers.
