Search published articles


Showing 2 results for Soosanabadi

Mohsen Soosanabadi Farahani, Kourosh Kamali, Masoud Karimlou, Mehdi Banan, Hamid Reza Khorram Khorshid,
Volume 16, Issue 6 (9-2013)
Abstract

Background: There is abundant evidence indicating that inflammatory mechanisms within the central nervous system contribute to cognitive impairment via cytokine-mediated interactions between neurons and glial cells. BAT1, a member of the DEAD-box family of RNA helicases, appears to regulate the production of inflammatory cytokines associated with AD pathology. In the current study BAT1 -22 promoter polymorphism was analyzed in AD and control subjects.

Materials and Methods: In this case-control study, genomic DNA from peripheral blood samples of 153 Alzheimer’s patients and 153 healthy controls was extracted using salting-out method. DNA analysis was performed by PCR-RFLP method and p<0.05 was considered statistically significant.

Results: After genotyping and statistical analysis the results failed to show any association between BAT1 -22 promoter polymorphism and sporadic Alzheimer’s disease.

Conclusion: BAT1 -22 is not associated with Alzheimer’s disease in Iranian population and so has no effect on predisposition to sporadic Alzheimer’s disease.


Tayyebeh Khoshbakht, Mohsen Soosanabadi, Masoud Karimlou, Maryem Neishaboury, Hamid Reza Khorram Khorshid,
Volume 17, Issue 7 (10-2014)
Abstract

Background: Interleukin-16 (IL16) is an important regulator of T cell activation and was reported to act as achemo-attractant agent. There are evidences that IL16 can control the neuroinflammatory processes in Alzheimer’s disease (AD). This study was performed to show whether the IL-16 genepolymorphism, rs11556218 is associated with the risk of sporadic AD in Iranian population.

Materials and Methods: Totally, 148 AD patients and 137non-dementia controls were recruited in this case-control study. Genotyping of rs11556218 T/Gpolymorphism was performed by PCR-RFLP method using the NdeI restriction enzyme.

Results: Statistical analysis of rs11556218 genotypes showed a protective effect against AD in the heterozygote genotype (p=0.001, OR=0.16(0.1-0.28)). Frequency of rs11556218 allele T was higher in patients than controls (p=0.001, OR=0.32(0.21-0.49)).

Conclusion: Our results indicate thatrs11556218 polymorphism has a protective role in the development of sporadic AD in Iranian population.



Page 1 from 1     

© 2025 CC BY-NC 4.0 | Journal of Arak University of Medical Sciences

Designed & Developed by : Yektaweb