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Rate of cognitive decline in AD is accelerated by the interleukin-1 -889 *1 allele

From the Department of Psychiatry and Behavioral Sciences (Drs. Murphy, Taylor, Tinklenberg, and Yesavage, and J. Claassen and N. Pascoe) and the Graduate Program in Immunology (J. DeVoss), Stanford University School of Medicine, CA; and the Department of Veterans Affairs Sierra–Pacific Mental Illness Research, Education, and Clinical Center (Drs. Murphy, Taylor, Tinklenberg, and Yesavage, and N. Pascoe), Palo Alto, CA.

Address correspondence and reprint requests to Dr. Greer Murphy, Neuroscience Research Laboratories, Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, CA 94305; e-mail: gmurphy{at}leland.stanford.edu

The reason for differences in rate of cognitive decline in AD is unknown. The interleukin-1 (IL-1) -889 *2 allele is associated with increased risk for AD. Surprisingly, in a sample of 114 patients followed for an average of 3.8 years, individuals homozygous for the IL-1 -889 *1 allele declined significantly more rapidly on the Mini-Mental State Examination than did others. There was no difference in rate of decline between patients with and without the APOE4 allele. These results support the hypothesis that inflammation is important in the clinical course of AD.

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