a1 School of Nursing, University of California, Los Angeles, U.S.A.
a2 Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, U.S.A.
a3 Department of Neurology, David Geffen School of Medicine, and UCLA Alzheimer's Disease Research Center, University of California, Los Angeles, U.S.A.
Background: While the relationship of apolipoprotein E (APOE) to behavioral symptoms of dementia (BSD) has been studied in community-dwelling persons with AD, it has received limited attention within the nursing home (NH) population. The aim of this study was to examine the association between APOE genotype and BSD in NH residents using direct observation.
Methods: Thirty-six participants, aged 71–102 years, were compared using a non-randomized two-group design with continuous measures. APOE genotype was obtained by buccal swab. BSD, including restlessness, escape restraint, tapping and banging, searching and wandering, pacing and walking, and vocalization, were measured using the Modified Agitated Behavior Rating Scale. Participants were observed every 20 minutes for 12 hours per day for five days. Each participant's mean behavior scores were compared according to the presence or absence of the APOE 4 allele.
Results: Resident characteristics included a mean MMSE of 10.44 indicating moderate to severe dementia and a mean of 3.44 medical co-morbidities. Fifty-six percent of the participants had one 4 allele. A significant difference was found between APOE 4+/4− and mean behavioral scores (F1,31 = 4.40, p = 0.04). Restlessness was significantly inversely correlated with MMSE (r = −0.367, p = 0.03), but not APOE genotype. There was no significant correlation between proxy reporting and direct observation (r = 0.257, p = 0.13).
Conclusion: Findings indicate that the presence of the APOE 4+ genotype increases the risk for BSD in NH residents with dementia. Direct observation proved a more accurate estimate of BSD than proxy report.
(Received August 06 2008)
(Revised October 09 2008)
(Revised February 23 2009)
(Accepted February 25 2009)
(Online publication May 27 2009)
c1 Correspondence should be addressed to: Diana Lynn Woods, Assistant Professor, University of California, Los Angeles, School of Nursing, 700 Tiverton Avenue, Box 956919, Los Angeles, CA 90095-6919, U.S.A. Phone: + 1 310 206-5457; Fax: +1 310 206-3241. Email: [email protected].