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Mortality in amnestic mild cognitive impairment

A prospective community study

From the Departments of Health Sciences Research (R.O.R., C.L.L., R.C.P., T.C.S.), Neurology (R.C.P., A.L.H.), Psychiatry and Psychology (Y.E.G., R.J.I.), and Internal Medicine (E.G.T.), Mayo Clinic College of Medicine, Rochester, MN.

Address correspondence and reprint requests to Dr. Ronald C. Petersen, Mayo Clinic, Department of Neurology, 200 First Street SW, Rochester, MN 55905; e-mail: peter8{at}mayo.edu).

Objective: To assess the hazard of death in persons with and without amnestic mild cognitive impairment (aMCI).

Methods: From 1987 through 2003, persons with aMCI (n = 243) and an age- and gender-matched reference group of cognitively normal persons in Olmsted County, MN, were recruited through the Mayo Clinic Alzheimer’s Disease Patient Registry and followed prospectively through 2004. Survival was estimated using Kaplan-Meier survival curves, and the hazard of death for the aMCI cohort vs the reference cohort was estimated using Cox proportional hazards models.

Results: Over a median follow-up of 5.7 years, persons with aMCI had increased mortality (hazard ratio [HR] = 1.7; 95% CI: 1.3 to 2.3) vs reference subjects. The hazard of death by aMCI subtype was 1.5 in persons with single-domain aMCI (95% CI: 1.1 to 2.1) and 2.9 in persons with multiple-domain aMCI (95% CI: 1.9 to 4.6) vs reference subjects. Analyses restricted to aMCI cases showed an interaction between aMCI subtype and APOE-4 allele status (p = 0.003). Among aMCI cases with an APOE-4 allele, there was no difference in mortality between single- and multiple-domain aMCI (HR = 1.2; 95% CI: 0.6 to 2.3). However, among aMCI cases with no APOE-4 allele, the hazard of death in multiple-domain aMCI was 4.6 (95% CI: 2.3 to 9.1) vs single-domain aMCI.

Conclusions: Amnestic mild cognitive impairment is associated with increased mortality, which is greater in multiple-domain aMCI than in single-domain aMCI. Mortality in aMCI subtypes may vary by APOE-4 allele status.

Supported by grants from the National Institutes of Health (P50 AG16574, and U01 AG06786, R01 AR30582, K01 MH68531) and by the Robert H. and Clarice Smith and the Abigail van Buren Alzheimer’s Disease Research Program.

Disclosure: The authors report no conflicts of interest.

Received December 21, 2005. Accepted in final form July 27, 2006.

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