Ccr2-64i and Ccr5 Δ32 Polymorphisms in Patients with Late-Onset Alzheimer’s disease; A Study from Iran (Ccr2-64i And Ccr5 Δ32 Polymorphisms in Alzheimer’s disease) | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 6، دوره 15، شماره 4، مهر 2012، صفحه 937-944 اصل مقاله (235.2 K) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2012.4882 | ||
| نویسندگان | ||
| Hamid Reza Khorram Khorshid1؛ Mehdi Manoochehri1؛ Leila Nasehi2؛ Mina Ohadi1؛ Mehdi Rahgozar3؛ Koorosh Kamali* 2 | ||
| 1Genetics Research Centre, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran | ||
| 2Reproductive Biotechnology Research Centre, Avicenna Research Institute (ACECR), Tehran, Iran | ||
| 3Epidemiology and Biostatistics Department, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran | ||
| چکیده | ||
| Objective(s) Alzheimer’s disease (AD) is a complex disease with multifactorial etiology. Inflammation has been proven to have an important role in the pathogenesis of AD. Both CCR2 and CCR5 genes expression increase in AD patients comparing to control subjects. CCR5 gene encodes a protein which is a member of the beta chemokine receptors family of integral membrane proteins. CCR5-Δ32 is a genetic variant of CCR5 and is characterized by the presence of a 32-bp deletion in the coding region of the gene, which leads to the expression of a nonfunctional receptor, and the CCR2-64I has a change of valine to isoleucine at codon 64, in the first transmembrane domain. It has been proved that both genes have important roles in different stages of inflammation. Materials and Methods The frequencies of CCR5∆32 and CCR2-64I variations were determined in 156 AD patients and 161 control subjects using polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods, and the results were compared among AD and healthy controls. Results Statistical analysis showed no significant difference in the distributions of CCR5∆32 and CCR2-64I between the AD patients and healthy controls (P> 0.05). Stratifying the samples by gender, genetic background and presence of ApoEε4 allele showed no significant effect on the distributions of CCR5∆32 and CCR2-64I (P> 0.05). Conclusion Our study did not show an association between CCR5∆32 and CCR2-64I variations and AD in the Iranian population. Further confirmatory studies with bigger number of samples are recommended. | ||
| کلیدواژهها | ||
| Alzheimer’s disease؛ Genetic Association study؛ CCR2؛ CCR5؛ Inflammation؛ Iranian Population | ||
| مراجع | ||
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