Rinsho Shinkeigaku (Clinical Neurology)

The 49th Annual Meeting of the Japanese Society of Neurology

Molecular epidemiology of cerebrovascular diseases; the Hisayama study and the Fukuoka Stroke Registry (FSR)

Takanari Kitazono, M.D.1), Michiaki Kubo, M.D.2), Jun Hata, M.D.3), Setsuro Ibayashi, M.D.4), Yutaka Kiyohara, M.D.3) and Mitsuo Iida, M.D.4)

1)Department of Nephrology, Hypertension, and Strokology, Kyushu University Hospital
2)Laboratory for Genotyping, SNP Research Center, The Institute of Physical and Chemical Research (RIKEN)
3)Department of Environmental Medicine, Graduate School of Medical Sciences, Kyushu University
4)Department of Medicine and Clinical Science, Graduate School of Medical Sciences, Kyushu University

The underlying pathogenesis of stroke is mediated by a variety of environmental risk factors as well as genetic ones. Thus, we have to evaluate the environmental factors precisely to identify the stroke-related gene polymorphisms. The Hisayama study, an epidemiological study of cardiovascular diseases, was established in 1961 in Hisayama, Japan. In 2002, a screening survey for the genetic study was performed in Hisayama. The Fukuoka Stroke Registry (FSR) is a hospital-based registration of stroke patients. Stroke specialists from eight medical centers in southern Japan have participated in FSR. In the present study, control and case subjects were recruited from the Hisayama study and FSR, respectively.
We performed a genome-wide case-control study and found that a nonsynonymous SNP in PRKCH encoding a member of protein kinase C (PKCη) was significantly associated with brain infarction. As a candidate gene analysis, we investigated the role of NAD (P) H oxidase C242T polymorphism in the development of brain infarction. The C242T polymorphism was not associated with lacunar and atherothrombotic infarction; however, the presence of T-allele may have a protective role in the occurrence of atrial fibrillation and cardioembolic brain infarction. These studies may provide important information for the development of the therapeutic strategies against stroke.
Full Text of this Article in Japanese PDF (408K)

(CLINICA NEUROL, 48: 892|895, 2008)
key words: brain infarction, single nucleotide polymorphism, protein kinase Cη, NAD (P) H oxidase

(Received: 16-May-08)