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(Stroke. 2005;36:179.)
© 2005 American Heart Association, Inc.

Advances in Stroke 2004

Update on the Genetics of Stroke and Cerebrovascular Disease 2004

From the Genetics of Vascular Disorders (E.T.-L.), CHU Lariboisière and INSERM E365, Paris, France; and the Department of Neurology (M.J.A.), Northwestern University Feinberg School of Medicine, Chicago, Ill.

Correspondence to Dr Mark J. Alberts, Director, Stroke Program, Department of Neurology, Northwestern University Feinberg School of Medicine, 710 N Lake Shore Dr, Chicago, IL 60611. E-mail m-alberts@northwestern.edu

Key Words: Advances in Stroke • intracranial aneurysm • subarachnoid hemorrhage

An extract of the first 250 words of the full text is provided, because this article has no abstract.

This year has again seen significant advances in our understanding of the genetic etiologies and pathogenesis for several types of stroke and cerebrovascular abnormalities. As in past years, there continues to be marked progress in understanding the genetic basis of hemorrhagic stroke, particularly those caused by aneurysms and cavernous malformations. In general, progress appears to be more substantial in the genetics of cerebral hemorrhage as compared with cerebral infarction. This may be because of the clarity of the phenotype, as well as a more defined role for genetics in some types of hemorrhagic stroke. Cerebral infarction is quite heterogeneous, with multiple risk factors (hypertension, diabetes, lipid disorders) playing complex roles in the pathogenesis of these types of stroke.¹ Despite these challenges, we have made progress in understanding the genetic of cerebral infarction.

The ascertainment of large numbers of families with intracranial aneurysms (IA) has led to significant linkage studies for this prodrome of subarachnoid hemorrhage. A Finnish study of 222 affected relative pairs with IAs found evidence for linkage near locus D19S246.² Several promising candidate genes are located around this locus. Another study involving families from Japan and Utah found evidence for linkage at locus D7S2421, which is near the elastin gene.³ Some previous studies have failed to confirm linkage of IA to elastin. Perhaps this reflects ascertainment issues to indicate genetic heterogeneity of the IA trait. A recent linkage study using a very large family with apparent autosomal dominant IAs identified a locus on chromosome 1p34–36.⁴ A recent study . . . [Full Text of this Article]

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