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Neurology 1999;52:1505
© 1999 American Academy of Neurology

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Brief Communications

A DLST genotype associated with reduced risk for Alzheimer’s disease

K.-F. R. Sheu, PhD, A. M. Brown, PhD, B. S. Kristal, PhD, R. N. Kalaria, FRCPath, L. Lilius, MA, L. Lannfelt, MD, PhD and J. P. Blass, MD, PhD

From the Burke Medical Research Institute (Drs. Sheu, Brown, Kristal, and Blass), Cornell University Medical College, White Plains, NY; the Alzheimer’s Disease Research Center and Pathology Institute (Dr. Kalaria), Case Western Reserve University, Cleveland, OH; and the Huddinge University Hospital (L. Lilius and Dr. Lannfelt), Karolinska Institute, Stockholm, Sweden.

Address correspondence and reprint requests to Dr. John Blass, Dementia Research Service, Burke Medical Research Institute, 785 Mamaroneck Avenue, White Plains, NY 10605; e-mail: jpblass{at}mail.med.cornell.edu

Recent studies suggest that variants of the DLST gene alter the risk of AD. DLST encodes the core subunit of the mitochondrial -ketoglutarate dehydrogenase complex, which is deficient in AD. The authors report that in 247 US white subjects, homozygosity for DLST A19,117, T19,183 was associated with a reduced risk of AD (odds ratio [OR] = 0.35, p = 0.018). The reduced risk was marked in subjects who did not carry the apolipoprotein (APOE)-4 allele (OR = 0.16, p = 0.014). Further study of DLST in AD appears warranted.