(Stroke. 1999;30:1881-1886.)
© 1999 American Heart Association, Inc.
Original Contributions |
Evaluation of Genetic Risk Factors for Silent Brain Infarction
From the Central Clinical Laboratory (Y.N.), Department of Laboratory Medicine (T.N., H-Y.P., J.M.), and the Third Department of Internal Medicine (S.K.), Shimane Medical University; and Shimane Institute of Health Science (T.N., S.K.), Izumo, Japan.
Correspondence to Toru Nabika, Department of Laboratory Medicine, Shimane Medical University, Izumo 693, Japan. E-mail nabika{at}shimane-med.ac.jp
Background and Purpose—Silent brain infarction (SBI) is often found with white matter hyperintensity. A recent genetic study on elderly twins indicated that the susceptibility to white matter hyperintensity was largely determined by genetic factors, implying the existence of genetic susceptibility for SBI as well. We therefore studied 3 genetic polymorphisms in SBI, the deletion/insertion polymorphism of angiotensin-converting enzyme (ACE) gene, the apolipoprotein(a) [apo(a)] size polymorphism, and the T677C polymorphism of methylenetetrahydrofolate reductase (MTHFR) gene, by a case-control study.
Methods—By MRI, 147 subjects with SBI and 214 without cerebral infarctions (control group) were selected from participants of a health examination of the brain. Seventy-four patients with symptomatic subcortical infarction (SSI) from the same area were also included in the study. In addition to the control group, 2 more reference populations were recruited. Typing of the apo(a) size polymorphism was done by Western blotting with the use of an anti-apo(a) antibody. Genotypes of ACE and MTHFR were determined by polymerase chain reaction amplification of the genomic DNA and subsequent restriction enzyme digestion.
Results—The ACE polymorphism was not associated with either SBI or SSI. In contrast, the small apo(a) was associated with both SSI and SBI. The MTHFR polymorphism was associated only with SSI. The association of MTHFR and apo(a) was greater in the younger subjects.
Conclusions—Among the 3 genetic polymorphisms studied, only the apo(a) size polymorphism is a risk factor for SBI.
Key Words: amine oxidoreductases • angiotensin converting enzymes • apolipoproteins • genetics • lacunar infarction
This article has been cited by other articles:
 |
|
 |
|
  S. Cronin, K. L. Furie, and P. J. Kelly Dose-Related Association of MTHFR 677T Allele With Risk of Ischemic Stroke: Evidence From a Cumulative Meta-Analysis Stroke, July 1, 2005; 36(7): 1581 - 1587. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Shibata, T. Nabika, H. Moriyama, J. Masuda, and S. Kobayashi Correlation of NO Metabolites and 8-Iso-Prostaglandin F2a With Periventricular Hyperintensity Severity Arterioscler Thromb Vasc Biol, September 1, 2004; 24(9): 1659 - 1663. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. L.P. Giele, T. D. Witkamp, W. P.T.M. Mali, Y. van der Graaf, and for the SMART Study Group Silent Brain Infarcts in Patients With Manifest Vascular Disease Stroke, March 1, 2004; 35(3): 742 - 746. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. T. Turner, C. R. Jack, M. Fornage, T. H. Mosley, E. Boerwinkle, and M. de Andrade Heritability of Leukoaraiosis in Hypertensive Sibships Hypertension, February 1, 2004; 43(2): 483 - 487. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. K. Kim, B. O. Choi, W. S. Jung, Y. J. Choi, and K. G. Choi Hyperhomocysteinemia as an independent risk factor for silent brain infarction Neurology, December 9, 2003; 61(11): 1595 - 1599. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Z Szolnoki, F Somogyvari, A Kondacs, M Szabo, L Fodor, J Bene, and B Melegh Evaluation of the modifying effects of unfavourable genotypes on classical clinical risk factors for ischaemic stroke J. Neurol. Neurosurg. Psychiatry, December 1, 2003; 74(12): 1615 - 1620. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Kohara, M. Fujisawa, F. Ando, Y. Tabara, N. Niino, T. Miki, and H. Shimokata MTHFR Gene Polymorphism as a Risk Factor for Silent Brain Infarcts and White Matter Lesions in the Japanese General Population: The NILS-LSA Study Stroke, May 1, 2003; 34(5): 1130 - 1135. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. J. Kelly, J. Rosand, J. P. Kistler, V. E. Shih, S. Silveira, A. Plomaritoglou, and K. L. Furie Homocysteine, MTHFR 677C->T polymorphism, and risk of ischemic stroke: Results of a meta-analysis Neurology, August 27, 2002; 59(4): 529 - 536. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Nasreen, T. Nabika, H. Shibata, H. Moriyama, K. Yamashita, J. Masuda, and S. Kobayashi T-786C Polymorphism in Endothelial NO Synthase Gene Affects Cerebral Circulation in Smokers: Possible Gene-Environmental Interaction Arterioscler Thromb Vasc Biol, April 1, 2002; 22(4): 605 - 610. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. M. Cupini, M. Diomedi, F. Placidi, M. Silvestrini, and P. Giacomini Cerebrovascular Reactivity and Subcortical Infarctions Arch Neurol, April 1, 2001; 58(4): 577 - 581. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Gallai, V. Caso, M. Paciaroni, G. Cardaioli, E. Arning, T. Bottiglieri, and L. Parnetti Mild Hyperhomocyst(e)inemia : A Possible Risk Factor for Cervical Artery Dissection Stroke, March 1, 2001; 32(3): 714 - 718. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. J. Tegos, E. Kalodiki, S.-S. Daskalopoulou, and A. N. Nicolaides Stroke: Epidemiology, Clinical Picture, and Risk Factors: Part I of III Angiology, October 1, 2000; 51(10): 793 - 808. [Abstract] [PDF]
|
|
|
|
 |
|
 P. M Ueland, H. Refsum, S. A. Beresford, and S. E. Vollset The controversy over homocysteine and cardiovascular risk Am. J. Clinical Nutrition, August 1, 2000; 72(2): 324 - 332. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Nasreen, T. Nabika, H. Shibata, H. Moriyama, K. Yamashita, J. Masuda, and S. Kobayashi T-786C Polymorphism in Endothelial NO Synthase Gene Affects Cerebral Circulation in Smokers: Possible Gene-Environmental Interaction Arterioscler Thromb Vasc Biol, April 1, 2002; 22(4): 605 - 610. [Abstract] [Full Text] [PDF]
|
|