Genetic association of TNF-α-308 G/A and -863 C/A polymorphisms with late onset Alzheimer’s disease in Azeri Turk population of Iran

Seiied Mojtaba Mohaddes Ardebili, Tarlan Yeghaneh, Jalal Gharesouran, Maryam Rezazadeh, Mehdi Farhoudi, Hormoz Ayromlou, Mahnaz Talebi, Morteza Ghojazadeh

Abstract


  • BACKGROUND: Recent findings suggest that production of pro-inflammatory cytokines, such as Tumour Necrosis Factor-alpha (TNF- α), is increased in the brain tissue of patients suffering late-onset Alzheimer’s disease (LOAD) and play an important role in the pathogenesis of this disease. Several epidemiological studies also suggest that patients taking anti-inflammatory drugs have a decreased risk of developing AD. TNF- α is an important pro inflammatory cytokine that is unregulated in Alzheimer’s patients. Functional polymorphisms in tumor necrosis factor alpha (TNF-α) can affect immune response, inflammation, tissue injury and possibly the susceptibility to Alzheimer disease (AD).
  • MÙETHODS: We used the polymorphic DNA markers (-308G/A) and (-863C/A) to study the association of TNF-α gene mutations with Late-onset Alzheimer’s disease (LOAD) and the relation between clinical features and genotypes in affected individuals. A total of 160 patient samples and 163 healthy controls from west northern Iran (Eastern Azerbaijan) were genotyped for the two polymorphisms by the PCR-RFLP method and genotype frequencies were statistically determined
  • RESULTS: Our data showed significant difference in TNF-α-308 G/A genotype and pro inflammatory cytokine allele frequencies between the Alzheimer disease patients and healthy subjects. Contrary to that, no significant difference was observed in TNF-α-863 C/A genotype and allele frequencies between these two groups
  • CONCLUSIONS:  TNF-α-308 G/A gene polymorphism could affect cerebral inflammatory response and the risk of late-onset Alzheimer disease but -863C/A polymorphism does not influence the risk of this disease and this possible association between TNF-α -308G/A and -863C/A gene polymorphisms have to be further elucidated in larger case control studies
  • KEYWORDS: Alzheimer, TNF- α, Polymorphism, PCR-RFLP, β-Amyloid, -308G/A, -863C/A

Keywords


Alzheimer; TNF-a; Polymorphism; PCR-RFLP; β-Amyloid, -308G/A; -863C/A

Full Text:

PDF XML