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Increased platelet membrane fluidity as a diagnostic marker for Alzheimer's disease

A test in population-based cases and controls

Department of Epidemiology, University of Washington, Seattle, WA (Dr. Kukull)
Department of Pharmacology, University of Washington, Seattle, WA (Dr. Hinds)
Department of Medicine (Neurology), University of Washington, Seattle, WA (Dr. Schellenberg)
Department of Biostatistics, University of Washington, Seattle, WA (Dr. van Belle)
Department of Medicine, University of Washington, Seattle, WA (Dr. Larson).

To test whether increased platelet membrane fluidity as measured by decreased steady state fluorescence anisotropy (r_s) of diphenylhexatriene is a biologic/diagnostic marker for Alzheimer's disease (AD), we enrolled 95 clinically diagnosed, probable AD cases from our Alzheimer's Disease Patient Registry and 133 control subjects of similar age and sex randomly selected from the same population base as the cases. We measured r_s in platelet membranes following published assay procedures. Laboratory personnel and investigators were blind to the identity of the samples; cases and controls were assayed in random order. Our analyses showed that the distributions of r_s values were unimodal and similar for cases and controls. The overall mean differences (control mean-case mean) for the two established assay methods tested were 0.0011 and 0.0003. A nonparametric Wilcoxon rank sum test also showed no difference between cases and controls. Multivariate analysis adjusted for the significant effects of the processing date and analysis platelet recovery led to a final model with the adjusted mean difference of 0.0007 for the principal method. Increased platelet membrane fluidity is not an antemortem diagnostic or biologic marker for AD in our population.

Address correspondence and reprint requests to Dr. W. A. Kukull, Department of Epidemiology, SC-36, University of Washington, Seattle, WA 98195.

Supported in part by National Institute of Aging grants R01 AG07584, U01 AG06781, and P50 AG05136.

Received May 21, 1991. Accepted for publication in final form August 21, 1991.

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