AI Article Synopsis
- Evidence shows that patients with Alzheimer's disease have higher oxidative DNA damage and reduced DNA repair capacity, specifically in the base excision repair pathway.
- 8-oxo-deoxyguanosine DNA glycosylase 1 (OGG1) is crucial for initiating the repair of oxidative damage, and variations in the OGG1 gene may affect repair effectiveness.
- A study found that Alzheimer's patients with the OGG1 Ser326Cys variant exhibited even greater oxidative DNA damage compared to those with the normal genotype, suggesting that this genetic polymorphism contributes to increased DNA damage in these patients.
Article Abstract
There is considerable evidence that oxidative DNA damage is increased, DNA repair capacity is decreased in patients with Alzheimer's disease. Base excision repair is the major pathway in removal of oxidative DNA damage. 8-oxo-deoxyguanosine DNA glycosylase 1 (OGG1) is the enzyme which is involved in the first step of this repair process. Alterations in DNA repair capacity may be related with polymorphisms in DNA repair genes. In order to investigate the effect of OGG1 Ser326Cys polymorphism on oxidative DNA damage level, OGG1 genotyping was performed, basal and oxidative DNA damage in lymphocytes and 8-OHdG level in plasma were examined in patients with Alzheimer's disease. Basal and oxidative DNA damage and 8-OHdG level were measured by OGG1-modified comet assay and enzyme-linked immunoassay, respectively. OGG1 genotyping was performed by polymerase chain reaction- restriction fragment length polymorphism assay. Basal and oxidative DNA damage and plasma 8-OHdG levels were found to be higher in the Alzheimer's disease group than those in the control group (P < 0.001). In the Alzheimer's disease group, the levels of oxidative DNA damage was higher in the patients having OGG1 (Ser326Cys + Cys326Cys) genotype than those in the patients having OGG1 Ser326Ser genotype. It was concluded that oxidative DNA damage is increased in patients with Alzheimer's disease and OGG1 Ser326Cys polymorphism may be responsible for this increase.
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| http://dx.doi.org/10.1016/j.neulet.2019.134362 | DOI Listing |
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