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Related Experiment Videos

Fibrinolytic gene polymorphism and ischemic stroke.

Katarina Jood1, Per Ladenvall, Anna Tjärnlund-Wolf

  • 1Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Göteborg, Sweden.

Stroke
|September 24, 2005
PubMed
Summary

Genetic variants in tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1) were not directly linked to ischemic stroke risk. However, a specific combination of tPA and PAI-1 genotypes showed a protective effect against stroke.

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Area of Science:

  • Genetics and Molecular Biology
  • Neurology
  • Cardiovascular Research

Background:

  • Tissue-type plasminogen activator (tPA) and plasminogen activator inhibitor type 1 (PAI-1) gene polymorphisms (-7351C>T and -675 4G>5G) affect gene activity.
  • These variants are linked to myocardial infarction, with T and 4G alleles increasing risk.

Purpose of the Study:

  • To investigate the association between tPA and PAI-1 polymorphisms and plasma protein levels with ischemic stroke.
  • To explore potential genetic risk factors for ischemic stroke.

Main Methods:

  • The Sahlgrenska Academy Study on Ischemic Stroke (SAHLSIS) included 600 ischemic stroke patients and 600 controls.
  • Stroke subtypes were classified using Trial of Org 10172 in Acute Treatment criteria.

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Main Results:

  • No significant association was found between individual tPA or PAI-1 genetic variants and ischemic stroke.
  • A protective effect was observed for the combined tPA CC/PAI-1 4G4G genotype (OR 0.65).
  • Elevated plasma levels of tPA and PAI-1 antigen were independently associated with ischemic stroke, with tPA levels varying by stroke subtype.

Conclusions:

  • Individual tPA and PAI-1 polymorphisms are not significantly associated with ischemic stroke.
  • The tPA CC/PAI-1 4G4G genotype combination demonstrated a protective effect.
  • These findings suggest a more intricate role for tPA and PAI-1 in cerebrovascular events compared to cardiac events.