TNFα, a significant immune mediator, may contribute to the initiation and progression of the ischemic stroke. Genetics of TNFα molecule may have an important role in the risk of ischemic stroke. The most interesting aspects of the G-308A polymorphism remain unexplained; there are many discrepancies between the results. Differences in the ethnicity of the studied cohorts may be taken as one of the possibility. Our study material consisted of 101 patients with ischemic stroke, including 30% classified as lacunar stroke. The diagnosis was based on the presence of rapidly developing neurological signs lasting longer then 24h and confirmed by neuroimaging matter. All patients were of Polish Caucasian origin. Randomly selected 100 individuals without any sign of the vascular disease of central nervous system were taken as the control material. The frequency of polymorphism G-308A in TNFα gene was determined as described by Rubattu et al. [11]. The genotype distribution in our material was similar and statistically insignificant between patients and controls. The heterozygotic G/A genotype was detected in 9% of patients and in 15% of control materials, homozygotic A/A was found in 5% of patients and only in one of control and G/G in 87% of patients and in 84% of control individuals. Our results are negative with respect to the impact of 308 TNFα polymorphism on the risk of ischemic stroke in Caucasians living in Poland.
A b s t r a c t Alzheimer disease (AD) is a complex, multi-factorial disease with the potential involvement of several genes. Alpha-2-macroglobulin (A2M) has been implicated in AD on the basis of its ability to mediate the clearance and degradation of β-amyloid peptide. Nevertheless, it is not clear whether there are racial differences in frequency of polymorphisms of A2M in AD. We examined a group of 50 unrelated patients from Poland (38 women and 12 men), who were diagnosed clinically as probably developing AD (according to the N1NCD3 -ADR PA criteria). The patients were examined by a neurologist and a psychologist and had a CT or MRI scan of the brain. Fifty individuals of matched age, withoutany signs of dementia, were studied as a control group. DNA was extracted by a routine method from a blood sample. Amplification and genotyping at A2M was performed as described by Blacker et al. (1997). The genotypic distribution in A2M exon 18 in patients with AD and genotype TT in A2M exon 24 was similar to that in the controls. Significant differences were noted only in early onset AD in males and for old onset disease in females. The deletions were found more frequently in AD; however, they were found in only a small proportion of studied patients. These findings indicate that A2M is not the only biological candidate gene for AD determination.
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