Our research group has been responsible for the identification of common genetic risk factors for both ischemic and developed methods two crucial methods with widespread application in the genetic investigation of complex diseases.

Related Publications

  1. Loci associated with ischaemic stroke and its subtypes (SiGN): a genome-wide association study

    The discovery of disease-associated loci through genome-wide association studies (GWAS) is the leading genetic approach to the identification of novel biological pathways underlying diseases in humans. Until recently, GWAS in ischaemic stroke have been limited by small sample sizes and have yielded few loci associated with ischaemic stroke. We did a large-scale GWAS to identify additional susceptibility genes for stroke and its subtypes.

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  2. Association Between Blood Pressure Control and Risk of Recurrent Intracerebral Hemorrhage

    Intracerebral hemorrhage (ICH) is the most severe form of stroke. Survivors are at high risk of recurrence, death, and worsening functional disability.  The goal of this study is to investigate the association between blood pressure (BP) after index ICH and risk of recurrent ICH.

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  3. Rare Coding Variation and Risk of Intracerebral Hemorrhage

    Intracerebral hemorrhage has a substantial genetic component. We performed a preliminary search for rare coding variants associated with intracerebral hemorrhage.  A meta-analyses of single-variant and gene-based association were computed.

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  4. APOE 4 and lipid levels affect risk of recurrent nonlobar intracerebral hemorrhage

    Genetic variants E2/E4 within the APOE gene are established risk factors for lobar intracerebral hemorrhage (ICH). Published preliminary data suggest a potential role for APOE E4 in risk of nonlobar ICH. We therefore investigated the role of APOE in recurrent nonlobar ICH, and sought to clarify whether effects of APOE on circulating lipids mediate this association.

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  5. Recommendations from the international stroke genetics consortium, part 1: standardized phenotypic data collection

    Majersik JJ, Cole JW, Golledge J, Rost NS, Chan YF, Gurol ME, Lindgren AG, Woo D, Fernandez-Cadenas I, Chen DT, Thijs V, Worrall BB, Kamal A, Bentley P, Wardlaw JM, Ruigrok YM, Battey TW, Schmidt R, Montaner J, Giese A, Roquer J, Jiménez-Conde J, Lee C,, Ay H, Martin JJ, Rosand J, Maguire J on behalf of theInternational Stroke Genetics Consortium. Recommendations from the international stroke genetics consortium, part 1: standardized phenotypic data collection. Stroke. 2015 Jan;46(1):279-84. PMID: 25492903; PMCID: PMC4465378.

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  6. The effect of survival bias on case-control genetic association studies of highly lethal diseases

    Anderson CD, Nalls MA, Biffi A, Greenberg SM, Singleton AB, Meschia JF, Rosand J. The effect of survival bias on case-control genetic association studies of highly lethal diseases. Circ Cardiovasc Genet 2011; 4(2): 188-196. PMID: 21292865. PMCID: PMC3080449

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  7. Principal-component analysis for assessment of population stratification in mitochondrial medical genetics

    Biffi A, Anderson CD, Rahman R, Nalls MA, Cortellini L, Rost NS, Plourde A, Sonni A, de Bakker PIW, Ross O, Greenberg SM, Furie KL, Meschia JF, Singleton AB, Saxxena R, Rosand J. Principal-component analysis for assessment of population stratification in mitochondrial medical genetics. American Journal of Human Genetics 2010;86:904-17. PMID: 20537299; PubMed Central PMCID: PMC3032075.

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  8. Many hypotheses but no replication for the association between PDE4D and stroke

    Rosand J, Bayley N, Rost N, de Bakker PI. Many hypotheses but no replication for the association between PDE4D and stroke. Nat Genet. 2006;38(10):1091-2. PubMed PMID: 17006457.

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  9. Human genome sequence variation and the search for genes influencing stroke

    Rosand J, Altshuler D. Human genome sequence variation and the search for genes influencing stroke. Stroke. 2003;34(10):2512-6. PMID: 14500931.

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