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Vascular factors and risk for neuropsychiatric symptoms in Alzheimer's disease: the Cache County Study

  • Katherine A. Treiber (a1), Constantine G. Lyketsos (a2), Chris Corcoran (a3), Martin Steinberg (a2), Maria Norton (a4), Robert C. Green (a5), Peter Rabins (a2), David M. Stein (a1), Kathleen A. Welsh-Bohmer (a6), John C. S. Breitner (a7) and JoAnn T. Tschanz (a1)
  • DOI: http://dx.doi.org/10.1017/S1041610208006704
  • Published online: 01 June 2008
Abstract
ABSTRACT

Objective: To examine, in an exploratory analysis, the association between vascular conditions and the occurrence of neuropsychiatric symptoms (NPS) in a population-based sample of incident Alzheimer's disease (AD).

Methods: The sample consisted of 254 participants, identified through two waves of assessment. NPS were assessed using the Neuropsychiatric Inventory. Prior to the onset of AD, data regarding a history of stroke, hypertension, hyperlipidemia, heart attack or coronary artery bypass graft (CABG), and diabetes were recorded. Logistic regression procedures were used to examine the relationship of each vascular condition to individual neuropsychiatric symptoms. Covariates considered were age, gender, education, APOE genotype, dementia severity, and overall health status.

Results: One or more NPS were observed in 51% of participants. Depression was most common (25.8%), followed by apathy (18.6%), and irritability (17.7%). Least common were elation (0.8%), hallucinations (5.6%), and disinhibition (6.0%). Stroke prior to the onset of AD was associated with increased risk of delusions (OR = 4.76, p = 0.02), depression (OR = 3.87, p = 0.03), and apathy (OR = 4.48, p = 0.02). Hypertension was associated with increased risk of delusions (OR = 2.34, p = 0.02), anxiety (OR = 4.10, p = 0.002), and agitation/aggression (OR = 2.82, p = 0.01). No associations were observed between NPS and diabetes, hyperlipidemia, heart attack or CABG, or overall health.

Conclusions: Results suggest that a history of stroke and hypertension increase the risk of specific NPS in patients with AD. These conditions may disrupt neural circuitry in brain areas involved in NPS. Findings may provide an avenue for reduction in occurrence of NPS through the treatment or prevention of vascular risk conditions.

Copyright
Corresponding author
Correspondence should be addressed to: Dr. JoAnn Tschanz, Center for Epidemiologic Studies, UMC 4440, Utah State University, Logan, UT 84322-4440, U.S.A. Phone: +1 435 797 8108; Fax: +1 435 797 2771. Email: joannt@cc.usu.edu.
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