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NEUROLOGY 2004;63:1711-1713
© 2004 American Academy of Neurology
Brief Communications

Alcohol dehydrogenase 2 variant is associated with cerebral infarction and lacunae

Y. Suzuki, MD, PhD, M. Fujisawa, MD, F. Ando, MD, PhD, N. Niino, MD, PhD, I. Ohsawa, PhD, H. Shimokata, MD, PhD and S. Ohta, PhD

From the Department of Biochemistry and Cell Biology (Drs. Suzuki, Ohsawa, and Ohta), Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, Kanagawa; Hokendohjin Medical Foundation (Dr. Suzuki), Chiyoda-ku, Tokyo; and Department of Epidemiology (Drs. Fujisawa, Ando, Niino, and Shimokata), National Center for Geriatrics and Gerontology, Obu, Aichi, Japan.

Address correspondence and reprint requests to Dr. Ohta, Department of Biochemistry and Cell Biology, Institute of Development and Aging Sciences, Graduate School of Medicine, Nippon Medical School, 1-396 Kosugi-cho, Nakahara-ku, Kawasaki, Kanagawa 211-8533, Japan; e-mail: ohta{at}nms.ac.jp

The authors examined the association of the alcohol dehydrogenase 2 (ADH2) genotype with vascular events in community-dwelling Japanese (1,102 men/1,093 women). The allele ADH2*2 encodes an isozyme with a higher level of activity than ADH2*1. Here, the authors show that the ADH2*1 carriage is associated with high prevalence of cerebral infarction and lacunae in men. Multiple regression analyses confirmed that the risk of lacunae and cerebral infarction was increased by the ADH2*1 allele.

Received March 25, 2004. Accepted in final form June 24, 2004.






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