Objectives: Several studies indicate that amyloid ß (Aß) peptide deposits and neurofibrillary tangles have key roles in pathogenesis and progression of the late-onset Alzhimer’s disease. Likewise it has been shown that inflammatory reactions play a significant role as well. Inflammatory mediators such as complement, chemokines and cytokines activators and inhibitors can release from activated microglia and astrocytes, causing neuronal dysfunction and death. One of the most important cytokines is tumor necrosis factor–α (TNF-α). This study was designed and carried out to determine the association between sporadic Alzheimer’s disease and the human TNF-α and APOE gene variations in Iranian population.

Methods & Materials: In this case-control study, the role of TNF-α gene polymorphism was determined in 167 sporadic AD patients and 163 healthy controls. Genomic DNA was extracted using standard salting out method from peripheral lymphocytes and TNF-α- 850C/T promoter polymorphism was genotyped using PCR/RFLP technique. Comparing the genotype and allelic frequencies were analyzed using chi-square and logistic regression tests by SPSS 11.5.

Results: The obtained results indicated that the frequency of TNF-α -850 heterozygote genotype (CT) was significantly higher in AD patients comparing healthy controls (P=0.038). Although no significant difference were observed in TNF-α -850 homozygote genotype (TT) and T allele between the studied groups. No interaction was shown between TNF-α -850 and APOE gene polymorphisms as well.

Conclusion: These data suggests the role of TNF-α -850 TC genotype as a risk factor for AD in Iranian population. Although to show the effects of homozygote genotype (TT) and T allele, a study with a larger sample size maybe indicated.

Objectives: Alzheimer’s disease is the most common kind of dementia in the old age, and its incidence increases with age. Previous studies have shown that cytokines are proteins that play an important role in inflammation, and their level changes in inflammatory diseases. Since Alzheimer’s disease is an inflammatory disease, cytokines may influence the occurrence of this disease. IL16 is a cytokine whose role has been proved in many inflammatory diseases. This gene is one of the coding genes of cytokines of the inflammatory process. It may be responsible for inflammatory pathology seen around old age plaques in Alzheimer’s disease. It can also associate with the pathology of Alzheimer’s disease. Therefore, the aim of this study was to investigate the effects of 2 polymorphisms of gene IL16 (rs1131445 and rs4072111) on the risk of patients diagnosed with Alzheimer’s disease in the Iranian population.
Methods & Materials: In this study, the intervention group consisted of 144 individuals who were diagnosed with Alzheimer’s disease by psychologists based on a clinical test (DSM-IV), and the control group included 173 healthy individuals with no psychological disorders. DNA was extracted by salting out technique. The PCR response was conducted (for replicating the mentioned pieces) for any polymorphism in optimized conditions by using designed primers. The product of PCR was first checked for the confirmation of accurate function of PCR using polyacrylamide gel electrophoresis (PAGE). Next, the PCR product was dissected by restriction fragment length polymorphism (RFLP) method with intended confining enzyme, and then the genotype of the samples was determined by PAGE. Individual genotypes were determined using the PCR-RFLP method. Statistical analyses were done using OpenEpi 2.3.1 and SPSS 11.5.
Results: The study of allelic analysis between the control and intervention groups by considering the confidence interval (CI=90%) and significant level (0.05) for rs1131445 showed that the C allele had no significant association with Alzheimer’s disease (P=0.656). The TC genotype did not show any significant difference with TT genotype (P=0.614). However, the study of allelic analysis for rs4072111 polymorphism between 2 groups showed that the relationship of T allele with the disease is significant, and this allele has a protective role in creating the disease (P=0.008). In addition, TC genotype as a protective status showed a significant association with Alzheimer’s disease (P=0.007).
Conclusion: The existence of polymorphism in some genes of the inflammatory pathway could make people susceptible to Alzheimer’s disease. The genetic changes in DNA sequence of gene IL16 could result in changes in cytokine product or its function. The association between rs4072111 and Alzheimer’s disease supports the presumptions and shows a probable role of this polymorphism in Alzheimer disease. Besides, the association between rs1131445 and Alzheimer disease cannot be proven due to the small number of samples (Power: 8.23%).

Objectives GSTs are detoxification enzymes that remove excess reactive oxygen species (ROS) from cells. Evidence suggests that oxidative stress plays a role in several stages of the neurodegenarative disease like Alzheimer disease. Free radicals and similar molecules are classified as reactive oxygen species (ROS), which can cause oxidative modifications in the cell. In this study we have investigated the association between GSTP1 (rs1695) and AD risk for  genetic variant in Iranian population.
Methods & Materials The patient group consisted of 280 cases for GSTP1 gene investigation, whose Alzheimer disease had been approved by psychologists based on clinical test (DSM-IV). The control group included 168 healthy individuals, satisfying the condition of not having any psychological disorders. Individuals’ genotype have been determined by PCR-RFLP method. Statistical analysis was done by logistic regression using OpenEpi 2.3.1 and SPSS 16.
Results Significant association was observed between heterozygote genotype (AG) rs1695 A/G of GSTP1 gene and the risk of Alzheimer disease (P=0.005, OR=0.57[0.38-0.84]).This genotype acts as a protective factor. This observed result was significant in within women group (P=0.02). Significant interaction was also found between heterozygote genotype (AG) rs1695 A/G of GSTP1 gene (protective factor) and absent ε4 allele in our study group (P=0.001).
Conclusion Based on our results, we suggest that heterozygote genotype (AG) rs1695 A/G of GSTP1 gene can act as a protective factor for Alzheimer disease in Iranian population.