The genetics of ischaemic stroke

Way out of my league, translation to my level please.
http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2009.02202.x/full
Only the abstract and future paragraphs are copied, you'll have to read the url to get totally confused.

Abstract.  Matarin M, Singleton A, Hardy J, Meschia J (Laboratory of Neurogenetics, Bethesda, MD, USA; UCL Institute of Neurology, London, UK; Mayo Clinic, Jacksonville, FL, USA). The genetics of ischaemic stroke (Review). J Intern Med 2010; 267: 139–155.

In this review, we discuss the genetic factors in both the aetiology and treatment of ischaemic stroke. We discuss candidate gene association studies, family linkage studies and the more recent whole genome association studies and whole genome expression studies. We also briefly discuss genetic testing for stroke risk and genetic analysis of treatment complications.

The future.  The coming months and years will see GWA studies of stroke and related phenotypes performed in multiple population samples, integrating analysis of SNPs, haplotypes and CNVs. As the sample sizes become larger the data will become more reliable and genuine and reproducible risk variants will be discovered. A subsequent challenge will be to move from these associated SNPs to a deeper understanding of the biology of risk for stroke. Many of the discovered susceptibility polymorphisms fall in noncoding regions and they are probably only tagging the real functional variants [112]. In future it will be necessary to move from association signal to causal variant, and from causal variant to the molecular and cellular mechanisms involved in generating phenotypic effects. There is a need for methodologies that allow both the interpretation of functional consequences of variants and the description of functionally important variants [113]. Linkage and association studies coupling expression with genetic variability data have started to reveal the genetics underlying part of this variation, including complex allele-specific interactions and its relatively high level of heritability [97, 113–116].

Integrating expression with genetic variability in human stroke targeting organs such as the brain and cerebral vessels could tell us about the causal variants of IS and how they lead to disease. Finally the next-generation whole-sequencing technologies will be able to explore genome that right now is inaccessible or unassayed, providing a better profile of genomic differences between cases and controls. Already commercialization of the meagre replicated findings is assuring, and whilst this is probably premature, it will undoubtedly continue to increase. Responsible use of the genetic data that comes from these risk analyses will pose a challenge both to the medical profession and to the public if we are to achieve the goal of well-organized personal medicine.