This Article Full Text Full Text (PDF) All Versions of this Article: 35/5/1061    most recent 01.STR.0000126476.10473.47v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Leys, D. Articles by Pasquier, F. Search for Related Content PubMed PubMed Citation Articles by Leys, D. Articles by Pasquier, F. Related Collections Clinical genetics Other hypertension Clinical Studies Epidemiology

(Stroke. 2004;35:1061.)
© 2004 American Heart Association, Inc.

Original Contributions

Editorial Comment—Not All Hypertensive Subjects Have Similar Risks for White Matter Lesions: Influence of Genetic Factors

Stroke and Memory Departments, Hôpital Roger Salengro, Lille, France

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

White matter lesions (WML) are frequently found on magnetic resonance imaging (MRI) scans in stroke patients, in patients with cognitive decline or dementia, and in healthy—usually elderly—subjects who have vascular risk factors, especially arterial hypertension.¹ However, many neurologists in their clinical practice have seen elderly subjects with a long history of improperly treated arterial hypertension who have only few WML. They have met also middle-aged subjects, with less severe, more recent, and properly treated arterial hypertension with already extensive WML. These clinical findings suggest that not all hypertensive subjects have similar risks of WML.

Genetic factors may explain differences in the susceptibility of the cerebral white matter to arterial hypertension: (1) cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is clearly identified as a genetic disease due to a mutation in the Notch 3 gene, in which severe WML occur at an early stage of the disease in young subjects, even in the absence of vascular risk factors;² (2) other genetic disorders may also lead to severe WML in the absence of vascular factors, eg, CARASIL (the R indicating recessive) and other nonNotch type angiopathies,³ familial amyloid angiopathies,⁴ hereditary endotheliopathy with retinopathy nephropathy and stroke,⁵ and cerebroretinal angiopathies;⁶ and (3) a greater correlation between the volumes of WML is observed between monozygotic twins than between dizygotic twins.⁷

Among the various genes that potentially predispose to WML in the presence of arterial hypertension, the apolipoprotein E (APOE) gene is one of the best candidates: (1) the APOE which is . . . [Full Text of this Article]