Stroke. 2004;35:2731-2734
Published online before print September 23, 2004,
doi: 10.1161/01.STR.0000143328.98154.33
(Stroke. 2004;35:2731.)
© 2004 American Heart Association, Inc.
Genomics-Proteomics and Stroke
Introduction
Katrina Gwinn-Hardy, MD
Valina Dawson, PhD
From the National Institute of Neurological Disorders and Stroke (K.G.-H.), National Institutes of Health, Bethesda, and Institute for Cell Engineering, Department of Neurology (V.D.), Johns Hopkins School of Medicine, Baltimore, Md.
Correspondence to Dr Katrina Gwinn-Hardy, 6001 Executive Blvd 2142, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. E-mail gwinnk@ninds.nih.gov
An extract of the first 250 words of the full text is provided, because this article has no abstract.
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Introduction
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Genetic causes of disease, including stroke, range from classic
mendelian (a single gene leads to disease) to complex (multiple
genes contribute to risk for disease in combination with other
genetic and/or environmental factors). One method of identifying
genetic risk factors is the candidate gene association study,
in which a given polymorphism in a gene of interest is compared
between cases or controls; if the polymorphism is more common
in affected subjects, a contribution to risk for disease is
implied. A candidate gene is usually selected because the gene
product is intuitively related to the disease process. Further
studies in other populations will reveal whether findings from
both association and candidate gene studies can be generalized.
Because stroke includes multiple clinically relevant subgroups,
the appropriate phenotyping approach is not yet known. It also
is unclear whether the biological factors contributing to risk
for one type of stroke are the same as those for the other types
or whether these are biologically differing entities. Medical
risk factors for stroke, such as hypertension, and shared risk
factors between stroke and cardiovascular disease, for example,
suggest that biological processes overlap across related disorders.
Despite the complex biological questions that remain to be answered
regarding stroke etiology and risk, genetic studies are of value
to elucidate risk factors for stroke, give us clues regarding
targets for interventional therapies, and give us insight into
the process leading to clinical stroke of all types.
Single gene disorders that cause stroke include hemoglobinopathies, dyslipoproteinemias, and cardioembolic disorders.1,2 Family . . . [Full Text of this Article]