Abstract
AimThe objective of this study was to explore the genetic association of myeloperoxidase (MPO) gene polymorphisms with risk of Alzheimer's disease (AD).MethodsBlood samples were collected from 116 AD patients and 134 age and gender matched healthy individuals. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was utilized to confirm MPO polymorphisms in promoter region. Plasma concentration of MPO was detected by enzyme-linked immuno sorbent assay. Genotype distributions of MPO polymorphisms were compared by χ2 test between the two groups. The status of linkage disequilibrium between MPO two polymorphisms was detected using Haploview. MPO concentrations were analyzed by non-parametric test.ResultsMPO rs2333227 polymorphism was positively associated with AD risk, especially under the AA+GA vs. GG and A vs. G genetic models (P=0.042, OR=1.719, 95%CI=1.017-2.906; P=0.041, OR=1.582, 95%CI=1.016-2.463). While, rs34097845 polymorphism significantly decreased the risk of AD, particularly GA and AA+GA genotypes (P=0.048, OR=0.555, 95%CI=0.308-0.998; P=0.042, OR=0.552, 95%CI=0.310-0.983). In addition, rs2333227 genotypes affected the plasma concentration of MPO. But for rs34097845 polymorphism, only GA genotype exhibited significant association with MPO concentration.ConclusionPolymorphisms in the promoter region of MPO distinctly contribute to AD risk possibly through regulating MPO concentration. Present results should be confirmed by further studies.
Highlights
Alzheimer19;s disease (AD) is one of the most common neurodegenerative diseases in old people
Polymorphisms in the promoter region of MPO distinctly contribute to AD risk possibly through regulating MPO concentration
Present results should be confirmed by further studies
Summary
Alzheimer19;s disease (AD) is one of the most common neurodegenerative diseases in old people. It is a long lasting disorder with irreversible process [1]. The clinical symptoms of AD are characterized by short-term memory loss, language disorder, and behavioural issues [3]. A lot of studies indicate that the major pathological characteristics of AD include abnormal deposition of amyloid beta (Aβ) and tau protein in brain, the loss of synapses and neurons, and the neurofibrillary tangles [6,7,8,9]. AD is a complex disease which is regulated by the genetic and environmental factors [14]. It is generally considered that the genetic factors, especially the key genes associated with the pathological characteristics, play a crucial role in AD [15]
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