Author/Authors :
Gozalpour, E Genetic Research Centre - University of Social Welfare and Rehabilitation Sciences, Tehran , Khorram Khorshid, HR Genetic Research Centre - University of Social Welfare and Rehabilitation Sciences, Tehran , Ohadi, M Genetic Research Centre - University of Social Welfare and Rehabilitation Sciences, Tehran , Kamali, K Dept. of Epidemiology and Biostatistics - Tehran University of Medical Sciences, Iran , Mohammd, K Dept. of Epidemiology and Biostatistics - Tehran University of Medical Sciences, Iran , Karimloo, M Dept. of Epidemiology and Biostatistics - University of Social Welfare and Rehabilitation Sciences, Tehran , Mirabzadeh, A Dept. of Psychiatry - University of Social Welfare and Rehabilitation Sciences, Tehran , Fotouhi, A Dept. of Epidemiology and Biostatistics - Tehran University of Medical Sciences, Iran
Abstract :
Background: Alzheimer’s disease as a neurodegenerative disorder is the commonest type of dementia. A growing number
of genes have been reported as the risk factors, which increase the susceptibility to Alzheimer’s disease. Apolipoprotein E
(APOE), which its !4 allele has been reported as a risk factor in late onset Alzheimer’s disease (AD), is the main cholesterol
carrier in the brain. The main goal of this study was to assess the role of APOE genotypes and alleles in AD in Iranian population.
Methods: This study was performed in Tehran, Iran from 2007 to 2008. Totally, 154 AD cases and 162 control subjects from
Iranian population were genotyped for APOE using PCR method. Genotype and alleles frequencies for APOE were calculated
and compared between AD case and control subjects by 42 or Fisher’s exact test. Type one error assumed less than 0.05.
Results: The frequency of !2!3 genotype was significantly higher in control subjects than AD patients was (13.5% versus
5.2%, P< 0.05) and !3!4 genotype frequency was significantly higher in AD cases compared with control subjects. APOE -!2
allele frequency in cases was lower than that of control subjects but this difference was not significant (4.2% versus 7.7%).
Conclusion: It seems that individuals carrying !4 allele, develop AD 6.5 times more than non-carriers do (OR= 6.566, 95%
CI= 2.89-14.92). It has been reported that !4 allele acts in dose- age-dependent manner but we have shown that the risk of
developing AD in male APOE -!4 allele carriers is higher than that of female !4 carriers.