Ccr۲-۶۴i and Ccr۵ Δ۳۲ Polymorphisms in Patients with Late-Onset Alzheimer’s disease; A Study from Iran (Ccr۲-۶۴i And Ccr۵ Δ۳۲ Polymorphisms in Alzheimer’s disease)

  • سال انتشار: 1391
  • محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 15، شماره: 4
  • کد COI اختصاصی: JR_IJBMS-15-4_006
  • زبان مقاله: انگلیسی
  • تعداد مشاهده: 294
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نویسندگان

Hamid Reza Khorram Khorshid

Genetics Research Centre, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran

Mehdi Manoochehri

Genetics Research Centre, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran

Leila Nasehi

Reproductive Biotechnology Research Centre, Avicenna Research Institute (ACECR), Tehran, Iran

Mina Ohadi

Genetics Research Centre, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran

Mehdi Rahgozar

Epidemiology and Biostatistics Department, University of Social Welfare and Rehabilitation Sciences, Tehran, Iran

Koorosh Kamali

Reproductive Biotechnology Research Centre, Avicenna Research Institute (ACECR), 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 CCR۲ and CCR۵ genes expression increase in AD patients comparing to control subjects. CCR۵ gene encodes a protein which is a member of the beta chemokine receptors family of integral membrane proteins. CCR۵-Δ۳۲ is a genetic variant of CCR۵ and is characterized by the presence of a ۳۲-bp deletion in the coding region of the gene, which leads to the expression of a nonfunctional receptor, and the CCR۲-۶۴I has a change of valine to isoleucine at codon ۶۴, 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 CCR۵∆۳۲ and CCR۲-۶۴I variations were determined in ۱۵۶ AD patients and ۱۶۱ 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 CCR۵∆۳۲ and CCR۲-۶۴I between the AD patients and healthy controls (P> ۰.۰۵). Stratifying the samples by gender, genetic background and presence of ApoEε۴ allele showed no significant effect on the distributions of CCR۵∆۳۲ and CCR۲-۶۴I        (P> ۰.۰۵). Conclusion Our study did not show an association between CCR۵∆۳۲ and CCR۲-۶۴I variations and AD in the Iranian population. Further confirmatory studies with bigger number of samples are recommended.

کلیدواژه ها

Alzheimer’s disease, Genetic Association study, CCR۲, CCR۵, Inflammation, Iranian Population

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