Abstract
Background Alzheimer’s disease (AD) may be caused by multiple factors, including genetics, age, environment etc. At present, AD associated genes are: gene App, ps1, ps2 and apoE. However, these associated genes account mainly for the abnormal increase and accumulation of Ab, rather than the molecular genetic mechanism for the formation of neurofibrillary tangles and neuronal loss. P35 is a neuron specific regulative unit of CDK5. p35 gene contain several SNPs, and at some SNPs sites, the change of as ingle base results in the corresponding change of P35 amino acids. Cleavage of P35 into P25 greatly increases the kinase activity of CDK5, which in turn abnormally phosphorylates tauprotein, and then contributes to the formation of neurofibrillary tangles. What we are interested in is whether the polymorphism of the P35 gene was involved in the pathogenesis of AD. There are few research reports about the relationship of the P35 gene polymorphism with AD. Methods
Highlights
Alzheimer’s disease (AD) may be caused by multiple factors, including genetics, age, environment etc
The polymerase chain reaction (PCR) products were examined through 2% agarose gel electrophoresis, and found that closely after the 250bp band existed a regular and clear band, which was the intended band of 260bp fragments of p35 gene including rs17852832 SNP
The purified fragments of 681-940bp of p35 gene including rs17852832 SNP were analyzed with method of restriction fragment length polymorphism (RFLP), and found that the p35 gene fragments of all cases of AD and controls were cut by Mva I into three shorter fragments, which length were 114bp, 90bp and 53bp
Summary
Alzheimer’s disease (AD) may be caused by multiple factors, including genetics, age, environment etc. AD associated genes are: gene App, ps, ps2 and apoE. These associated genes account mainly for the abnormal increase and accumulation of Ab, rather than the molecular genetic mechanism for the formation of neurofibrillary tangles and neuronal loss. P35 gene contain several SNPs, and at some SNPs sites, the change of a single base results in the corresponding change of P35 amino acids. Cleavage of P35 into P25 greatly increases the kinase activity of CDK5, which in turn abnormally phosphorylates tauprotein, and contributes to the formation of neurofibrillary tangles. What we are interested in is whether the polymorphism of the P35 gene was involved in the pathogenesis of AD. There are few research reports about the relationship of the P35 gene polymorphism with AD
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