We used logistic regression, adjusted for demographics, apolipoprotein E ɛ4, heart rate, mean arterial pressure, and select cardiovascular risk factors, to estimate the odds of lacunar infarcts or cerebral microbleeds.
Of the infarction subtypes, PRKCH1425G/A was associated with lacunar infarction (OR = 1.8, 95% CI: 1.1-2.9, p = 0.025), which remained significant when adjusted for co-variables (OR = 2.0, 95% CI: 1.1-3.5, p = 0.015).
Recently, a large-scale genetic epidemiological study has shown significant association of single nucleotide polymorphisms (SNPs) in the protein kinase C eta (PRKCH) gene with cerebral infarction, particularly, with lacunar infarction.
Here we report that a nonsynonymous SNP in a member of protein kinase C (PKC) family, PRKCH, was significantly associated with lacunar infarction in two independent Japanese samples (P = 5.1 x 10(-7), crude odds ratio of 1.40).
Apo E genotypes were not related to the pathological type of stroke (cerebral infarction, CI, n = 532 and primary intracranial haemorrhage, PICH, n = 60, (chi2 =3.738, 4 d.f., P=0.44) nor with the Oxfordshire Community Stroke Project Classification subtypes of cerebral infarction, lacunar infarction, LACI (n = 169), total anterior circulation infarction, TACI (n = 117), partial anterior circulation infarction, PACI (n = 173), posterior circulation infarction, POCS (n = 54) and including those cerebral infarcts which could not be classified (n= 19), chi2 =31.1, 20 d.f., P=0.153).
Notch3 extracellular domain (N3ECD) accumulates in arterial walls followed by VSMC degeneration and subsequent fibrosis and stenosis of arterioles, predominantly in cerebral white matter, where characteristic ischemic MRI changes and lacunar infarcts emerge.
Some features were significantly (Fisher exact test p < 0.05) more frequent in CADASIL than in NOTCH3-negative patients: history of migraine (73 vs 39%), stroke before the age of 60 among relatives (71 vs 32%), severe leukoencephalopathy (94 vs 62%), white matter changes extended to the anterior temporal lobes (93 vs 45%), external capsule involvement (100 vs 50%), and presence of lacunar infarcts (100 vs 65%).
Furthermore, the ACE gene polymorphism was significantly different between symptomatic patients with a single lacuna and asymptomatic subjects with 4 or more multiple lacunar infarctions (chi(2) = 10.6, p = 0.005).
We used the following four candidate gene polymorphisms: angiotensin converting enzyme (ACE)/Insertion(I)-Deletion(D), angiotensinogen (AGT)/M235T, angiotensin II type 1 receptor (AT1)/ A1166C, type 2 receptor (AT2)/C3123A, to examine the association between polymorphisms and the severity of lacunar infarction.
There were no significant differences in the distributions of ACE genotypes and alleles between the patients with lacunar infarcts and with cortical infarcts in all ages.
Periodontitis was independently associated with increased levels of IL-6 (R<sup>2 </sup> = 0.656, P < 0.001), PTX3 (R<sup>2 </sup> = 0.115, P < 0.001), sTWEAK (R<sup>2 </sup> = 0.527, P < 0.001), and Aβ<sub>1-40</sub> (R<sup>2 </sup> = 0.467, P < 0.001) in patients with LI.
Intron 4aa genotype of eNOS gene seems to be protective for isolated LI and the effect was potentiated by the absence of 786C polymorphism in any allele of the promoter region.
We determined the role of 3 potentially functional eNOS polymorphisms (T-786C, intron 4ab, G894T) located toward the 5' flanking end of the gene as risk factors for SVD and different SVD subtypes: isolated lacunar infarction (n=137) and ischemic leukoaraiosis (n=160).
We used the following four candidate gene polymorphisms: angiotensin converting enzyme (ACE)/Insertion(I)-Deletion(D), angiotensinogen (AGT)/M235T, angiotensin II type 1 receptor (AT1)/ A1166C, type 2 receptor (AT2)/C3123A, to examine the association between polymorphisms and the severity of lacunar infarction.