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Published online before print September 14, 2005, doi:10.1212/01.wnl.0000178744.42953.b7)
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Received March 24, 2005
Accepted July 12, 2005

Familial aggregation, the PDE4D gene, and ischemic stroke in a genetically isolated population

M. J.E. van Rijn MSc, A. J.C. Slooter MD, PhD, A. F.C. Schut MD, PhD, A. Isaacs DSc, Y. S. Aulchenko PhD, P. J.L.M. Snijders MD, L. J. Kappelle MD, PhD, J. C. van Swieten MD, PhD, B. A. Oostra PhD, and C. M. van Duijn PhD*

From the Departments of Epidemiology and Biostatistics (Ms. van Rijn and Drs. Slooter, Schut, Isaacs, Aulchenko, Snijders, and van Duijn), Neurology (Dr. van Swieten), and Clinical Genetics (Dr. Oostra), Erasmus Medical Center, Rotterdam; Departments of Intensive Care and Neurology, Academic Medical Center, Amsterdam (Dr. Slooter); and Rudolf Magnus Institute for Neuroscience, Department of Neurology, University Medical Center, Utrecht, The Netherlands (Dr. Kappelle).


* To whom correspondence should be addressed. E-mail: c.vanduijn{at}erasmusmc.nl.

Abstract-- Objective: The purpose of this investigation was to study the familial aggregation of ischemic stroke and the association between the PDE4D gene and ischemic stroke. Methods: The study was performed in an isolated population in The Netherlands, where the authors identified 91 patients with ischemic stroke. Ischemic stroke was subclassified in large- and small-vessel infarction. The authors calculated kinship and inbreeding coefficients and genotyped all patients for three single-nucleotide polymorphisms (SNPs) in the PDE4D gene. Results: The proportion of related pairs was higher in patients with ischemic stroke (68.8%) compared with controls (30.7%; p < 0.001). For large-vessel infarction, the proportion of related pairs was higher (71%) compared with small-vessel infarction (62.8%; p < 0.001). Familial aggregation was strongest for patients with early onset (age at onset <45 years). All stroke groups were significantly more inbred compared with controls. In inbred individuals, the C allele of SNP45 increased the risk of small-vessel infarction 4.8 times (95% CI 1.1 to 22.3) compared with controls (p = 0.04). The T allele of SNP39 increased the risk of small-vessel infarction 6.3 times (95% CI 1.4 to 28.7) compared with controls (p = 0.02). No associations were found for large-vessel stroke. Conclusions: There was familial aggregation of ischemic stroke and a difference in degree of familial clustering between stroke subtypes. The authors also found that the PDE4D gene is significantly associated with small-vessel infarction in inbred individuals.




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